Tag Archives: alzheimer’s

Amazon indigenous people barely get dementia. Could a pre-industrial lifestyle protect against Alzheimer’s?

Nearly 1 in 10 Americans over the age of 65 have dementia, and as the U.S. struggles with an aging population, the proportion of elderly people with Alzheimer’s and other neurodegenerative diseases is bound to increase. But in the Amazon basin, where some indigenous people still employ a subsistence lifestyle as they have for hundreds of years isolated from industrialized society, the rate of dementia hovers at around just 1%. These findings, reported by a new study from the University of South California, suggest that the Western lifestyle may be seriously putting people at risk of dementia in old age.

“Something about the pre-industrial subsistence lifestyle appears to protect older Tsimane and Moseten from dementia,” said Margaret Gatz, the lead study author and professor of psychology, gerontology and preventive medicine at the University of South California.

The Tsimane have little or no access to health care but are extremely active and consume a high-fiber diet that includes vegetables, fish and lean meat. (Photo/Courtesy of the Tsimane Health and Life History Project Team)

Gatz and colleagues traveled to the Bolivian Amazon jungle, where they closely studied the elderly of the Tsimane’ and Mosetén tribes — two indigenous peoples that have remained largely isolated from urban life elsewhere in the country.

The Tsimane’ number about 16,000 people living in mostly riverbank villages scattered across about 3,000 square miles of the Amazon jungle. They are forager-farmers who fish, hunt, and cut down trees with machetes, which keeps everyone very physically active throughout their lifetimes.

The neighboring Mosetén, which number around 3,000 and have close cultural ties with the Tsimane’, also reside in rural villages and rely on subsistence agricultural work. However, they live closer to towns, have schools, and access to health posts, as well as access to roads and electricity. Within the last decade, the Mosetén have also received cell phone service and running water.

Researchers employed computer tomography (CT) brain scans, cognitive and neurological tests, and questionnaires to assess the mental health among the Tsimane’ and Mosetén aged 60 and over.

According to the results, the study found just 5 cases of dementia among 435 Tsimane’ and one case among 169 Mosetén, which is much less than the rate of incidence in Western countries. Previously, studies of indigenous populations in Australia, North America, Guam, and Brazil found dementia prevalence ranging from 0.5% to 20%. The authors note that the apparent higher rate of dementia among older adults from indigenous tribes elsewhere in the world could be due to their higher contact with their industrialized neighbors, and subsequent adoption of more sedentary lifestyles.

In the same over-60 groups, the researchers also diagnosed about 8% of elderly Tsimane’ and 10% of Mosetén with mild cognitive impairment (MCI) — the stage between the expected cognitive decline of normal aging and the more serious decline of dementia. This condition is characterized by memory loss and a decline in cognitive abilities, such as language and spatial reasoning. The MCI rates were comparable to those encountered in high-income countries.

In high-income countries with high rates of dementia among older adults, the population generally does not engage in the recommended amount of physical activity and has a diet rich in sugars and fats. As a result, older adults are more susceptible to heart disease and brain aging. In contrast, the Tsimane’ people have unusually healthy hearts for their age. That’s not surprising considering they also have the lowest prevalence of coronary atherosclerosis of any population in the world.

Alzheimer’s has been previously associated with hypertension, diabetes, cardiovascular diseases, physical inactivity, and even air pollution. It’s no coincidence that these chronic diseases and health problems are staples of modern Western lifestyles.

In 2021, the same team from the University of South California found that the Tsimane indigenous people of the Bolivian Amazon experience less brain atrophy than their American and European peers. Their decrease in brain volume happened at a rate that was 70% lower than in Western populations.

“We’re in a race for solutions to the growing prevalence of Alzheimer’s disease and related dementias,” said Hillard Kaplan, a study co-author and professor of health economics and anthropology at Chapman University who has studied the Tsimane for two decades. “Looking at these diverse populations augments and accelerates our understanding of these diseases and generates new insights.”

If the Tsimane’ and Mosetén offer any indication, a pre-industrial lifestyle can offer significant protection against dementia. But that doesn’t mean we can all revert to foraging in the woods and living under the stars. In case someone is romanticizing life in the Amazon jungle, bear in mind that the Tsimane’ have an average of nine children per family who live an average of just over 50 years compared to the world average of 71.5 years. So while it may be true that indigenous Amazon people rarely suffer from dementia at old age, what’s certain is that even fewer actually make it that far.

The findings were published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association.

Solving crosswords and number puzzles may make your brain sharper at old age

Regular use of word and number puzzles may help keep our brains working better for longer. According to a pair of studies, adults aged 50 and over who are in the habit of solving crosswords and Sudoku scored much higher on cognitive tests, such as those that assess problem-solving and memory, than those who didn’t. In some instances, the differences were quite dramatic: people who regularly do puzzles had the cognitive abilities of those eight years younger, on average, compared to those who didn’t.

Credit: Pixabay.

Researchers led by Dr. Anne Corbett of the University of Exeter Medical School surveyed participants in the PROTECT study, a large online cohort of over 22,000 older adults between the ages of 50 and 96, about how frequently they engage in word and number puzzles. The participants then had to undertake a battery of cognitive tests whose results are supposed to measure age-related changes in brain function. These include tasks that assess attention, reasoning, and memory. The results were striking.

Those who engage in crosswords had a brain function equivalent to ten years younger than their biological age on tests assessing grammatical reasoning and eight years younger than their age on tests measuring short-term memory.

“The improvements are particularly clear in the speed and accuracy of their performance. In some areas the improvement was quite dramatic — on measures of problem-solving, people who regularly do these puzzles performed equivalent to an average of eight years younger compared to those who don’t. We can’t say that playing these puzzles necessarily reduces the risk of dementia in later life but this research supports previous findings that indicate regular use of word and number puzzles helps keep our brains working better for longer,” Corbett said in a statement.

PROTECT is designed as a 25-year study and participants are followed-up yearly to assess how their brain ages and what lifestyle choices might influence the risk of dementia later in life. Despite tremendous progress, we still know little about how the brain ages or what causes debilitating neurodegenerative diseases like Alzheimer’s or Parkinson’s. PROTECT may offer exciting research opportunities in the year to come.

The two studies published in the International Journal of Geriatric Psychiatry don’t necessarily conclude that solving puzzles will necessarily reduce the risk of dementia and keep your brain sharper. The findings are observational and it could just be that people who have a natural ability to preserve their brain function with age also have a tendency to use word and numbers puzzles. In other words, the study established a correlation but did not define causation.

However, the findings are consistent with previous studies. A 2011 experiment with participants from the Bronx Aging Study found regularly solving crosswords is associated with a delay in the onset of cognitive decline. Other studies came to totally different conclusions. When Scottish researchers tested nearly 500 participants, all born in 1936, and found a tricky crossword or a challenging puzzle will not fend off age-related mental decline. However, they did note that although brain games like jigsaw puzzles may not prevent dementia, regularly challenging yourself mentally seems to improve the brain’s ability to cope with neurodegenerative disease.

“We know that what is good for the heart is good for the head, and there are other ways we can reduce our risk of developing dementia,” James Pickett, head of research at the UK’s Alzheimer’s Society, told CNN, “by taking steps towards a healthy lifestyle, eating a balanced diet, avoiding smoking and heavy drinking, and exercising regularly.”

If you want to keep your brain healthy, paying attention to your diet is clearly shown to help, but the occasional puzzle can’t hurt either.

Machine learning tool 99% accurate at spotting early signs of Alzheimer’s in the lab

Researchers at the Kaunas Universities in Lithuania have developed an algorithm that can predict the risk of someone developing Alzheimer’s disease from brain images with over 99% accuracy.

Image credits Nevit Dilmen via Wikimedia.

Alzheimer’s is the world’s leading cause of dementia, according to the World Health Organization, causing or contributing to an estimated 70% of cases. As living standards improve and the average age of global populations increase, it is very likely that the number of dementia cases will increase greatly in the future, as the condition is highly correlated with age.

However, since the early stages of dementia have almost no clear, accepted symptoms, the condition is almost always identified in its latter stages, where intervention options are limited. The team from Kaunas hopes that their work will help protect people from dementia by allowing doctors to identify those at risk much earlier.

Finding our early

“Medical professionals all over the world attempt to raise awareness of an early Alzheimer’s diagnosis, which provides the affected with a better chance of benefiting from treatment. This was one of the most important issues for choosing a topic for Modupe Odusami, a Ph.D. student from Nigeria,” says Rytis Maskeliūnas, a researcher at the Department of Multimedia Engineering, Faculty of Informatics, Kaunas University of Technology (KTU), Odusami’s Ph.D. supervisor.

One possible early sign of Alzheimer’s is mild cognitive impairment (MCI), a middle ground between the decline we could reasonably expect to see naturally as we age, and dementia. Previous research has shown that functional magnetic resonance imaging (fMRI) can identify areas of the brain where MCI is ongoing, although not all cases can be detected in this way. At the same time, finding physical features associated with MCI in the brain doesn’t necessarily prove illness, but is more of a strong indicator that something is not working well.

While possible to detect early-onset Alzheimer’s this way, however, the authors explain that manually identifying MCI in these images is extremely time-consuming and requires highly specific knowledge, meaning any implementation would be prohibitively expensive and could only handle a tiny amount of cases.

“Modern signal processing allows delegating the image processing to the machine, which can complete it faster and accurately enough. Of course, we don’t dare to suggest that a medical professional should ever rely on any algorithm one-hundred-percent. Think of a machine as a robot capable of doing the most tedious task of sorting the data and searching for features. In this scenario, after the computer algorithm selects potentially affected cases, the specialist can look into them more closely, and at the end, everybody benefits as the diagnosis and the treatment reaches the patient much faster,” says Maskeliūnas, who supervised the team working on the model.

The model was trained on fMRI images from 138 subjects from The Alzheimer’s Disease Neuroimaging Initiative fMRI dataset. It was asked to separate these images into six categories, ranging across the spectrum from healthy through to full-onset Alzheimer’s. Several tens of thousands of images were selected for training and validation purposes. The authors report that it was able to correctly identify MCI features in this dataset, achieving accuracies between 99.95% and 99.99% for different subsets of the data.

While this is not the first automated system meant to identify early onset of Alzheimer’s from this type of data, the accuracy of this system is nothing short of impressive. The team cautions that “such high numbers are not indicators of true real-life performance”, but the results are still encouraging, and they are working to improve their algorithm with more data.

Their end goal is to turn this algorithm into a portable, easy-to-use software — perhaps even an app.

“Technologies can make medicine more accessible and cheaper. Although they will never (or at least not soon) truly replace the medical professional, technologies can encourage seeking timely diagnosis and help,” says Maskeliūnas.

The paper “Analysis of Features of Alzheimer’s Disease: Detection of Early Stage from Functional Brain Changes in Magnetic Resonance Images Using a Finetuned ResNet18 Network” has been published in the journal Diagnostics.

Your brain is cleaning itself while you’re dreaming, new research suggests

The findings help us better understand why virtually all animals sleep, despite the fact that it leaves us helpless against predators and other threats.

Image via Pixabay.

The team, led by members from the University of Tsukuba explains that a certain phase of sleep (rapid eye movement sleep, or REM) gives our brains the opportunity to perform necessary maintenance. This, in turn, ensures that they’re running at peak capacity the rest of the time. The research builds on previous measurements of blood flow in the brain during different phases of sleep and wakefulness, which yielded conflicting results. In this study, the researchers used a technique to directly visualize how red blood cells move through the brain capillaries of sleeping and awake mice, while also measuring electrical activity in the brain.


“We used a dye to make the brain blood vessels visible under fluorescent light, using a technique known as two-photon microscopy,” says senior author of the study Professor Yu Hayashi. “In this way, we could directly observe the red blood cells in capillaries of the neocortex in non-anesthetized mice.”

“We were surprised by the results. There was a massive flow of red blood cells through the brain capillaries during REM sleep, but no difference between non-REM sleep and the awake state, showing that REM sleep is a unique state”

In order to help elucidate the confusing previous findings around this topic, the authors monitored brain flow rates in different areas of the brain alongside electrical activity. The latter was used to distinguish between different states of awareness (non-REM sleep, REM sleep, full wakefulness). Since we know that the development of certain conditions such as Alzheimer’s — which involve the buildup of waste products in the brain — is associated with reduced blood flow in the brain, the former was used as a rough estimate for maintenance and cleaning processes taking place in the mice’s brains.

The link between the two is that the removal of these waste products involves biochemical processes that eventually culminate in an increased blood flow (as the waste needs to be physically removed) during rest. Disposal of this material doesn’t take place, to the best of our knowledge, during wakefulness; or, at least, not to any extent that we’ve been able to pick up on.

After recording the differences between the three states, the team also disrupted the mice’s sleeping. They report that this resulted in their brains engaging in a “rebound” REM sleeping pattern later in the experiment. This state, which resembles a stronger REM sleeping state, was likely used to compensate for the earlier disruption, the team hypothesizes. This, by itself, suggests that REM sleep has an important role to play in brain functionality.

Later, the team repeated this sleep disruption experiment with mice whose brain A2a receptors were artificially blocked — these are the same receptors that get blocked after you have a cup of coffee, and doing so makes you feel more awake. In these conditions, they saw a much lower increase in blood flow during both REM and rebound-REM sleep. This is a strong indicator “that adenosine A2a receptors may be responsible for at least some of the changes in blood flow in the brain during REM sleep,” says Professor Hayashi.

Judging from these findings, the team says that there may be merit in investigating whether the heightened blood flow seen in brain capillaries during REM sleep facilitates waste removal from brain tissues. This could, in time, lead us towards treatments or preventive measures against conditions such as Alzheimer’s disease. They also point to adenosine A2a receptors as a prime candidate for such treatments, given the observed role of these neurons in modulating blood flow in the brain during REM sleep.

The paper “Cerebral capillary blood flow upsurge during REM sleep is mediated by A2a receptors” has been published in the journal Cell Reports.

Dementia cases estimated to triple worldwide by 2050, as populations and average age increase

Although better education and access to health services in developed countries have and will keep reducing the incidence of dementia, the number of people who suffer from it worldwide will triple by 2050, according to new estimates.

Image via Pixabay.

New research from the Health Metrics and Evaluation at the University of Washington School of Medicine estimates that the incidence of dementia worldwide will triple by 2050, with most new cases being concentrated in sub-Saharan Africa, North Africa, and the Middle East. Smoking, high body mass index, and high blood sugar will be the leading causes of this rise, it explains, while improved living conditions in developed countries will lower overall incidence in these areas.

All in all, dementia cases by 2050 would reach more than 152 million worldwide, according to the estimates.

“Improvements in lifestyle in adults in developed countries and other places — including increasing access to education and greater attention to heart health issues — have reduced incidence in recent years, but total numbers with dementia are still going up because of the aging of the population,” said Maria C. Carrillo, Ph.D., Alzheimer’s Association chief science officer. “In addition, obesity, diabetes and sedentary lifestyles in younger people are rising quickly, and these are risk factors for dementia.”

Today, roughly 1 in every 10,000 people worldwide develops early-onset dementia, which is dementia that sets in before the age of 65. This corresponds to roughly 350,000 new cases per year globally. But its effects are not evenly distributed: even in countries such as the US, the mortality rate from Alzheimer’s (the leading cause of dementia) is highest in rural areas compared to the richer, more developed urban centers.

But it’s not a US-only problem. In order to estimate future trends in dementia onset on a country-by-country basis, the team used data from 1999 to 2019 from the Global Burden of Disease (GBD) study, which estimated health trends worldwide and aimed, in part, to improve previous forecasts by incorporating information on trends in dementia risk factors.

According to them, dementia cases will increase from an estimated 57.4 (50.4 to 65.1) million cases globally in 2019 to an estimated 152.8 (130.8 to 175.6) million cases in 2050. Sub-Saharan Africa, North Africa, and the Middle East will likely see the greatest increases. Overall, however, most of these new cases will come down to population growth and an overall higher average age. Lifestyle factors such as smoking, high body mass index (BMI), and high blood sugar will also increase the prevalence of dementia, to the tune of an estimated 6.8 million cases worldwide by 2050. However, improvements in education levels, healthcare quality, and healthcare access will mostly cancel these out, removing an estimated 6.2 million possible cases.

“These estimates will allow policymakers and decision makers to better understand the expected increases in the number of individuals with dementia as well as the drivers of these increases in a given geographical setting,” Nichols said. “The large anticipated increase in the number of individuals with dementia emphasizes the vital need for research focused on the discovery of disease-modifying treatments and effective low-cost interventions for the prevention or delay of dementia onset.”

“Without effective treatments to stop, slow or prevent Alzheimer’s and all dementia, this number will grow beyond 2050 and continue to impact individuals, caregivers, health systems and governments globally,” said Maria C. Carrillo, Ph.D., Alzheimer’s Association chief science officer. “In addition to therapeutics, it’s critical to uncover culturally-tailored interventions that reduce dementia risk through lifestyle factors like education, diet and exercise.”

With lengthening lifespans around the world, the influence of education and healthcare on the incidence of Alzheimer’s and dementia becomes ever-more powerful. The team reports that there is “an increasing discrepancy in Alzheimer’s mortality” between urban and rural areas of the US and, very likely, in other areas of the world. Lower socioeconomic status, higher average levels of chronic disease, limited availability of internet services, and less access to health services (including primary care) account for most of this difference, the team explains.

We can deduce from here that there is also a disparity in incidence between developed and developing countries from similar, if not the same, causes.

The paper “Estimating the global mortality from Alzheimer’s disease and other dementias: A new method and results from the Global Burden of Disease study 2019” has been published in the journal Alzheimer’s & Dementia.

New blood test can determine who’s at risk of Alzheimer’s years before symptoms begin

A newly-developed blood test could help tell who’s at risk of developing Alzheimer’s before the onset of symptoms.

Image credits Mohamed Hassan.

The research focused on patients who were clinically diagnosed as not having Alzheimer’s, but perceived themselves as being cognitively impaired — a condition known as Subjective Cognitive Decline, SCD. The goal was to see whether a new type of test could tell which of these patients were at risk of developing Alzheimer’s later on.

So far, the findings are very encouraging: the test managed to pinpoint during the study all 22 subjects who developed Alzheimer’s dementia, thus the clinical symptoms, within six years. It further identified those participants who were at very low risk of developing it as well.

Testing for the future

The authors, a joint German-Dutch research team worked with 203 participants, taking samples of their blood and analyzing these through an immuno-infrared sensor for misfolding of the amyloid-beta (Aβ) peptides — a known biomarker for Alzheimer’s disease. They were also extensively tested for Alzheimer’s, proving that none of the participants had developed the condition at the study’s onset.

However, testing revealed misfolded Aβ peptides at this point in 22 participants, all of whom developed clinical Alzheimer’s in the six years after the study. For patients with mild misfolding, onset of clinical Alzheimer’s took longer on average (3.4 years) than for subjects with severe Aβ misfolding (2.2 years).

The researchers used these figures to predict the risk of each participant developing clinical Alzheimer’s disease using a statistical model. This suggested that participants with SCD and mild misfolding have an 11-fold higher risk of developing the condition, while those with SCD and severe misfolding were 19 times as likely to develop clinical Alzheimer’s than the other participants.

“Misfolding of Aβ is therefore a very precise prognostic plasma biomarker,” concludes  biophysics Professor Klaus Gerwert from the Bochum Research Center for Protein Diagnostics, lead researcher of the paper.

They further checked whether their predictions could be improved by looking at the combination of two different measurement methods for Alzhimer’s biomarkers — the level of misfolding of all Aβ isoforms alongside the ratio of Aβ42 to Aβ40 in plasma. This did increase the accuracy of the predictions statistically, the team explains.

“We can now very accurately predict the risk of developing clinical Alzheimer’s disease in the future, with a simple blood test on symptom-free individuals with subjective concerns,” explains Gerwert. “However, we can just as confidently give the all-clear for SCD patients who have a very low probability of developing Alzheimer’s disease in the next six years.”

The test can also be used to “monitor disease progression over 14 years”, starting frim the asymptomatic stage all the way to clinical onset, says Julia Stockmann of the Bochum Research Center for Protein Diagnostics, co-lead author of the paper.

Such a test is an essential half of a working strategy against Alzheimer’s. Once we’re able to actually treat the condition (there are some drugs in the works that may serve this purpose, such as aducanumab, still in testing with the U.S. Food and Drug Administration), such a test can be used to tell who is most in need of treatment, potentially saving thousands of lives from a debilitating condition.

“Our results indicate that Alzheimer’s drugs should be applied as early as possible in a non-clinical stage to improve therapy response,” Gerwert said.

The paper “Amyloid-β misfolding as a plasma biomarker indicates risk for future clinical Alzheimer’s disease in individuals with subjective cognitive decline” has been published in the journal Alzheimer’s Research & Therapy.


Hypertension treatment may stave off dementia in some patients

Researchers found that improving vascular health in people aged 50 or older could also have benefits for the brain. According to an exciting new study, patients who underwent intense treatment for hypertension were less likely to develop minor cognitive and memory problems — the kind that often progresses into dementia at old age — than patients who received standard care.


Credit: Pixabay.

The research was part of a broader cardiovascular study called Sprint, which began in 2010 and involved more than 9,000 people with hypertension across 102 sites in the United States. High blood pressure, also called hypertension, is dangerous because it makes the heart work harder to pump blood out to the body. The condition is diagnosed when a person has a systolic blood pressure between 130 and 180 and, if left unchecked, can lead to hardening of the arteries, stroke, heart failure, and other medical problems

The main goal of Sprint was to see whether people who received intensive treatment that lowered their blood pressure to 120 were doing significantly better than those who received standard treatment which lowered their blood pressure to around 140. These participants were also cognitively assessed.

In the three years following the study, those who had blood pressure below 120 were 19% less likely to develop mild cognitive impairment than those who received standard care. Additionally, blood pressure treatments significantly lowered the risk of stroke and death, as reported in the Journal of the American Medical Association (JAMA).

Dementia is the loss of cognitive functioning — thinking, remembering, and reasoning — and behavioral abilities to such an extent that it interferes with a person’s quality of life. One of the most important diseases that cause dementia is Alzheimer’s, which affects 6 million Americans.

There is no cure for Alzheimer’s but since the disease is preceded by mild cognitive impairment, the new findings suggest that keeping blood pressure in optimal parameters might stave off dementia or at least delay it considerably. Researchers might know for sure in future studies that follow patients who have received blood pressure treatment for a longer time.

Until then, patients with blood pressure over 130 shouldn’t hurry to talk to their doctors about lowering it even further. There is still much we need to find out about how results differ by age and the side effects. But, since the results have been so promising, the Alzheimer’s Association announced that it will award more than $800,000 to support a follow-up trial. In 2019, another research team found convincing evidence that gum disease may be gradually causing Alzheimer’s.

What causes dementia and how to keep it at bay

If you were to travel 40 years into the past, you’d rarely see people talk about dementia. It was often regarded as a fact of life — instances of incapacity and memory loss were usually considered as a normal part of aging for which ‘nothing’ could be done. Today, things are different and that’s just not good enough.

As the stigma associated with mental illnesses is slowly challenged, increased awareness and interest from health services have brought dementia more and more into the spotlight, which is an important driver for finding new ways of treating and dealing with dementia.

Credit: Pixabay.

The fatalistic view that surrounds dementia

The way society thinks about a disease is pretty important. When you think there is no cure for it, what’s the point in doing something about it? That’s an unfortunate way of looking at things, which can have significant repercussions in the long run.

Although there is no technical cure for dementia, that doesn’t mean there is no way to prevent or manage this disease. Better diet, enhanced cardiovascular health and better educational qualifications are all good options to reduce your risk of dementia. Having an overall healthy lifestyle is generally the best way to go about it.

Other scientific findings suggest that the prevalence of dementia can be indicative of public health in general. Though we don’t know the impact of all the involved factors, studying the impact of physical inactivity, obesity and diabetes on dementia would well give us a point towards a certain direction. Research has shown that diabetes can increase the risk of developing both Alzheimer’s disease and vascular dementia, and the two are often interrelated.

Although dementia awareness is moving into a generally positive direction, we should also be careful and consider the devastating consequences of this disease and the dire need of assisted care till the end of life. People are living longer than ever, and as a result, the rates of dementia are also increasing. No matter what the figures may suggest about declining figures of dementia prevalence, it is certainly true that dementia is on the rise as there will be a large number of older people suffering from it in the near future.

What Causes Dementia – The Science

The exact mechanisms of dementia still hold some secrets, but researchers have a pretty good idea of how it works. Toxic levels of urea inside the brain are mainly responsible for damaging the parts of the brain which leads to dementia — a neurodegenerative disorder that causes cognitive impairment.

Urea is a by-product of protein metabolism that is produced within the liver in order to filter ammonia from the human body. It is excreted from the body in the form of urine after it is filtered by kidneys.

However, the causes of dementia are much more varied, and include things such as vascular impairment, Parkinson’s disease, and most commonly, Alzheimer’s. But that’s hardly all.

According to a study recently published by scientists from Australia, UK, US, and New Zealand, Huntington’s disease is one of the 7 major forms of dementia that is associated with aging. This disease has got a direct link to the human brain’s urea levels and also the metabolic processes. In fact, there was another study in 2016 that linked urea with the development of Alzheimer’s.

However, scientists also added that there is way more research needed to have a clear idea on the way the urea levels elevate. The present study was done on the brains of human beings that were generously donated by families for medical reasons, as well as on the brains of sheep that were modified genetically. The study included scientists from the University of Auckland, Manchester, New Zealand, and the South Australian Research and Development Institute.

Dementia is a killer

There’s currently no cure for vascular dementia. There is also no way to reverse any damage that occurred before the treatment commenced — but there is a treatment. Sometimes, the treatment can be effective at slowing down the damage and tackling the underlying cause of dementia.

Nevertheless, dementia is a killer.

Both directly and indirectly, dementia can claim lives. Since it is essentially a degeneration in the cerebral cortex, the part of the brain responsible for thoughts, memories, actions, and personality, it can cause numerous cascading issues down the road.

Migraines are also connected

Recent research has also found that migraines are an important risk factor for dementia. Multiple reports from different sources have said that migraine attacks are one of the main issues for Americans, Brits, and Australians but the long term impact on this health condition is still unknown. There are several results that show that focusing attention to migraines in dementia and Alzheimer’s is warranted to get a full clear idea about what migraine is and how it sets the stage for dementia if it is not treated in the long run.

A survey involving 680 seniors who didn’t have any past experience of cognitive issues asked them about their history of migraines. More than half of the respondents of the survey were women and their average age was 76. After they were tracked for 5 years, researchers found that 55 among them developed dementia. If other factors like age and education were taken into account, those who had Alzheimer’s and dementia were 5 times more likely to have experienced migraine attacks.

On the other hand, people with a history of migraines were thrice more likely to develop a kind of dementia and more than 4 times more likely to develop Alzheimer’s, which is one of the biggest causes of dementia. Moreover, the reason that was figured out for linking dementia with migraine attacks were poor lifestyle decisions, not spending an active life and not following a healthy diet. These are already known reasons for aggravating dementia risk.

Scientists need more research to conclude whether or not the disruption in various lifestyle factors like diet, exercising, and mental stimulation also plays a pivotal role in raising the risk of dementia. Not taking proper care of cardiovascular health is yet another reason that can heighten the chances of dementia in the long run.

Effective treatments for dementia – Is it possible to find a cure?

Researchers, from all over the globe, are all working together to develop the most effective treatments that could treat dementia, if not to find out a proper cure.

Currently, there is no potential cure for Alzheimer’s disease. But the medicines that are available now can not only improve the quality of life but also stop the progress of dementia. In the following part of this post, we’ll discuss the few treatments that are associated with Alzheimer’s disease.

#1: Immunotherapy and Alzheimer’s vaccine

Researchers have been trying hard for more than a decade to develop an effective vaccine that could prevent Alzheimer’s disease. As long as immunotherapy is concerned, the strategy behind this is to utilize the immune system of the body to destroy beta-amyloid plaques. An approach to developing a vaccine is by utilizing immunoglobulin which consists of antibodies. This has been shown to be successful among people who had mild Alzheimer’s disease, in the earlier stages of the condition. Though this trial can be deemed to be too small, it suggests that immunoglobulin therapy may have safety benefits over other techniques of vaccination.

#2: Paliatives

No, there is still no medicine that could cure dementia but there are definitely some that might help a patient with treating some symptoms for some time. Doctors might recommend other medicines to treat issues brought in by dementia, such as insomnia, depression or extreme irritation without any reason. A physician might recommend:

Memantine controls a chemical in the brain that is required for memory and learning. They often combine it with donepezil for treating moderate to severe dementia.

Anxiolytics like Ativan or Serax can ease off restlessness and anxiety

Antidepressants, particularly selective serotonin reuptake inhibitors can reduce irritability and bad mood issues

Antipsychotic medicines like Abilify, Haldol, Risperdal, Zyprexa can exert control on behaviors and feelings like agitation, aggression, hallucinations, and delusions.

#3: Therapeutic treatments

The therapeutic approaches can jolt your ailing family member’s memory and improve their thinking abilities. The therapies usually make sure that anything that they try will keep them from feeling frustrated or overwhelmed.

Reminisce therapy: This includes speaking with your family members and friends about your school days, hometown, favorite hobbies, and pleasant memories from work life. This therapy can both be done one-on-one or in a group.

Cognitive stimulation therapy: CST is a rather structured program that helps people who are suffering from the mild-to-moderate stage of dementia. The therapist engages you in activities, like speaking on current events, singing songs, cooking by looking at a recipe, playing word games or crossword puzzles.

Reality orientation training: This therapy deals with basic information like the person’s name, the time and date of the day. There are few patients that find this therapy to be too very patronizing. In case you see this method to not work on your loved one, don’t force it on him.

Reverse memory loss – Few changes to bring about in your daily life

You can’t remember where you kept your car keys? Did you just forget what you had to buy from the grocery store? You can’t remember the name of your physical trainer whom you spoke to three days back at the gym? If yes, you’re not alone. While everyone forgets things at times yet memory loss shouldn’t be taken too lightly especially when it is linked with dementia.

Don’t forget to include physical activity in your routine

Physical activity boosts blood flow to your entire body and brain and this keeps your memory sharp. The Department of Health and Human Services advise you to spend at least 150 minutes in a week in some form of activity like brisk walking, aerobic activity, jogging or 75 minutes of vigorous activity. If you’re too busy and you don’t have time for a full session of workout, you should take out 10 minutes for walking every day.

Socialize and stay in touch with people

Just as we all know that social interaction is something that wards of stress and depression, it can also work wonders in curing memory loss. Watch out for opportunities to socialize with your friends, loved ones and others. Stay away from living alone as they say, ‘an idle mind is a devil’s workshop.’

Try to stay mentally active

Physical activity helps your body stay in shape, but there are other mentally stimulating tasks that can also keep your brain in proper shape and help you reverse memory loss. You can play card games like bridge or crossword puzzles. While driving to a destination, take alternate routes so that you can tax your brain in finding new ways. Volunteer at a school organization and community.

Stay organized and systematic

When your home is cluttered, you’ll most likely forget things more than what you would have if your home was organized. You have to bring about a slight change in your lifestyle by getting systematic with things so that you keep yourself from forgetting. If you have appointments, note them down, write down a to-do list every morning or use an electronic planner that can remind you things. Tick off the items that you’ve already completed and try to keep your to-do lists current.

Opt for a healthy diet

This is not the first time we’re talking about the benefits of a healthy diet, and it’s no coincidence. While it is definitely good for your physical health, it is equally good for your mental health. Try and choose low-fat sources of protein like beans, fish and skinless poultry. Don’t drink too much alcohol as this can lead to memory loss.

Dementia is on the rise in many countries all over the globe — taking steps to reduce its risk is crucial. The sooner you start, the more effective it is.


The first symptom of Alzheimer’s is excessive sleepiness

New research at UC San Francisco shows that Alzheimer’s disease directly attacks brain regions responsible for wakefulness during the day.


Image via Pixabay.

Both researchers and caregivers have noted that Alzheimer’s patients can develop excessive daytime napping long before showing the memory problems associated with the disease, the paper reads. Prior studies have considered that this is just a symptom of poor nighttime sleep caused by Alzheimer’s-related disruptions in the brain regions that govern sleep, while others have argued that the sleep problems themselves contribute to the progression of the disease.

However, the new study comes to show that this is in fact caused by Alzheimer’s itself.

Sleepy brain

“Our work shows definitive evidence that the brain areas promoting wakefulness degenerate due to accumulation of tau — not amyloid — protein from the very earliest stages of the disease,” said study senior author Lea T. Grinberg, MD, Ph.D., an associate professor of neurology and pathology at the UCSF Memory and Aging Center.

The brain regions that govern sleep  (including the part of the brain impacted by narcolepsy) are among the first to degrade at the onset of Alzheimer’s disease, the team reports. Therefore, excessive daytime napping, particularly when it occurs in the absence of significant nighttime sleep problems, could serve as an early warning sign of the disease.

The findings also add to the body of evidence suggesting that tau proteins contribute more directly to the brain degeneration that drives Alzheimer’s symptoms than the more extensively studied amyloid protein.

Led by lead author Jun Oh, a Grinberg lab research associate, the team measured Alzheimer’s pathology, tau protein levels, and neuron numbers in three brain regions involved in promoting wakefulness. The team used a sample of 13 deceased Alzheimer’s patients and seven healthy control subjects, which were obtained from the UCSF Neurodegenerative Disease Brain Bank.

The brains of Alzheimer’s patients had significant tau buildup in all three wakefulness-promoting brain centers compared to the healthy controls, the team reports. These three areas were the locus coeruleus (LC), lateral hypothalamic area (LHA), and tuberomammillary nucleus (TMN). The same regions had lost as many as 75% of their neurons, the team adds.

“It’s remarkable because it’s not just a single brain nucleus that’s degenerating, but the whole wakefulness-promoting network,” Oh said. “Crucially this means that the brain has no way to compensate because all of these functionally related cell types are being destroyed at the same time.”

Oh’s team also studied brain samples from seven patients with progressive supranuclear palsy (PSP) and corticobasal disease (CBD), two distinct forms of neurodegenerative dementia caused by tau accumulation. These brains didn’t show any loss of neurons in the same three areas despite showing significant tau protein build-ups.

“It seems that the wakefulness-promoting network is particularly vulnerable in Alzheimer’s disease,” Oh said. “Understanding why this is the case is something we need to follow up in future research.”

The work also ties in with previous research by Grinberg’s team, which showed that people who died with elevated levels of tau protein in their brainstem — i.e. in the earliest stages of Alzheimer’s disease onset — had already begun to experience changes in mood, such as anxiety and depression, as well as increased sleep disturbances.

“Our new evidence for tau-linked degeneration of the brain’s wakefulness centers provides a compelling neurobiological explanation for those findings,” Grinberg said. “It suggests we need to be much more focused on understanding the early stages of tau accumulation in these brain areas in our ongoing search for Alzheimer’s treatments.”

The paper “Profound degeneration of wake-promoting neurons in Alzheimer’s disease” has been published in the journal  Alzheimer’s and Dementia.

Credit: Pixabay.

New studies explain why many more women than men are affected by Alzheimer’s

Credit: Pixabay.

Most people caring for and supporting people with Alzheimer’s are also women. Credit: Pixabay.

Women are disproportionately affected by Alzheimer’s disease (AD) — nearly two-thirds of the 5 million Americans living with Alzheimer’s are women. The biological underpinnings for these sex-based differences have been somewhat of a mystery — until recently. New studies may have unraveled some of the biological mechanisms that make women so much more vulnerable to the debilitating disease.

It’s not just because women live longer

Alzheimer’s is the most common type of dementia. The symptoms of Alzheimer’s disease generally start off mild, which makes early diagnosis difficult, but they get worse over time and start to interfere with daily life more and more.

In the early stages, the damage is confined to the entorhinal cortex and hippocampus, two areas associated with memory, navigation, and perception of time. This sort of degeneration leads to memory loss and disorientation associated with the condition — though it has to be noted that Alzheimer’s starts damaging brain cells well before the first symptoms kick in.

Alzheimer’s disease is widely believed to be caused by the accumulation of beta-amyloid proteins which clump together to form plaques between neurons and disrupt cell function. Another physical characteristic of the Alzheimer’s diseased brain is the buildup of tau proteins, which tangle inside neurons, blocking their transport system.

Women live more than men in most countries around the globe, but that doesn’t explain the disproportionate amount of women affected by Alzheimer’s at any age. Previous studies have suggested that there are genetic and biologic factors that may raise the risk of developing the disease in women.

Scientists, for instance, have found associations between a gene called APOE-4 and a higher risk of Alzheimer’s for women than men in certain age groups. Also, women tend to do better on verbal tests than men, which can mask the symptoms of the disease in its early stages.

In a series of new studies presented at the Alzheimer’s Association International Conference in Los Angeles on Tuesday, researchers claim they’ve found new clues that may explain these gender-based differences.

“Understanding these sex-specific differences may help us identify and apply customized prevention strategies for different populations against cognitive decline, Alzheimer’s disease and other dementias,” Maria Carrillo, chief science officer from the Alzheimer’s Association, said in a statement.

Researchers at Vanderbilt University scanned the brains of 301 people with no cognitive impairment and 161 individuals with mild impairments, mapping where tau proteins were deposited. These tau maps were overlaid onto nerve networks — highways that brain signals follow. The analysis revealed that tau deposits in women with mild impairment were more diffuse and spread out than in men, affecting more areas of the brain.

Elsewhere, at the University of California, San Diego, researchers analyzed more than 1,000 brain scans of older adults, which showed differences in how each gender uses sugar in the brain. Apparently, women metabolize sugar better, which may give them an edge in verbal skill tests that can compensate for some of the damage from dementia — at least initially in the disease’s early phases.

Finally, researchers at the University of Miami analyzed the genes of over 30,000 people, half with Alzheimer’s, half without it. They identified four genes that seem to be associated with sex-based differences in Alzheimer’s incidence. One of the genes confers risk in female and not males and three confer risk in males but not females. However, the research team still doesn’t know how exactly these genes affect risk.

“This research demonstrates that genetics may contribute to differences in risk and progression of Alzheimer’s disease between men and women,” says Brain Kunkle, a genetic epidemiologist from the University of Miami working on the study. “More research is needed to understand how much these genes contribute to Alzheimer’s risk, and whether they can be used to specifically identify men and women at risk for this disease.”

Credit: Pixabay.

Researchers test Alzheimer’s vaccine in mice

Credit: Pixabay.

Credit: Pixabay.

Researchers successfully tested a vaccine that targets a protein that builds up in the brains of people affected by Alzheimer’s. The vaccine has so far been tested only a mice but the researchers hope that their highly positive results will help them receive fundings for a clinical trial involving humans soon.

Finally, a vaccine for Alzheimer’s disease?

After a certain age, the human brain starts to shrink considerably but surprisingly, not too many neurons die in the process. In the Alzheimer’s diseased brain, however, many neurons stop functioning, lose connections with other neurons, and eventually die. The progressive disorder is the main cause of dementia and affects a third of senior citizens, or roughly 43 million people worldwide.

In the early stage, the damage is confined to the entorhinal cortex and hippocampus, two areas associated with memory, navigation, and perception of time. This sort of degeneration leads to memory loss and disorientation associated with the condition — though it has to be noted that Alzheimer’s starts damaging brain cells well before the first symptoms kick in.

Alzheimer’s disease is widely believed to be caused by the accumulation of beta-amyloid proteins which clump together to form plaques between neurons and disrupt cell function. Another physical characteristic of the Alzheimer’s diseased brain is the buildup of tau proteins, which tangle inside neurons, blocking their transport system.

Since 2013, researchers at the University of New Mexico (UNM) led by Dr. Kiran Bhaskar have been working on a vaccine that targets tau proteins, in the hope that it might prevent the progression of Alzheimer’s.

The vaccine was used on a group of mice that had Alzheimer’s-like symptoms. The vaccine’s antibodies seem to have cleared out pathological tau which tangles the brains of patients with Alzheimers’ disease. This response lasted for months, the researchers reported in the journal NPJ Vaccines.

Tau proteins are normally a stabilizing structure in the brain — it’s the long tangles that disrupt the ability of neurons to communicate with one another.

“We’re excited by these findings, because they seem to suggest that we can use the body’s own immune system to make antibodies against these tangles,” said Nicole Maphis, a Ph.D. candidate in UNM’s Biomedical Sciences Graduate Program.

In order to determine the vaccine’s efficacy, the researchers had mice go through maze-like tests. The rodents that received the vaccine were significantly better at navigating the mazes than those that didn’t receive the vaccine.

Scientists had also used monkeys and rabbits in their testing and hope to soon to validate the vaccine on humans if they receive enough funding. It’s common for drugs that work on mice or other animals not to have the same effect in humans, so a healthy dose of skepticism is advised.

“We have to make sure that we have a clinical version of the vaccine so that we can test in people,” Bhaskar said.

Brushing your teeth could prevent Alzheimer’s and other diseases

Three days into Alzheimer’s and Brain Awareness Month, two new studies have proven that good dental hygiene can do more than just give you a pretty smile and freshen your breath. Turns out it could probably save your life.

Credit: Pixabay.

An Alzheimer’s study earlier this year discovered that the bacteria causing gingivitis can move from the mouth to the brain where the enzymes they excrete can destroy the nerve cells in the brain, leading to the deadly disease. However, a new study from the University of Bergen is the first to identify DNA evidence of it doing so. In the study of 53 people with the condition, 96 percent tested positive for the enzyme.

“We discovered DNA-based proof that the bacteria causing gingivitis can move from the mouth to the brain,” says researcher Piotr Mydel at Broegelmanns Research Laboratory, Department of Clinical Science, University of Bergen.

But Mydel does state that it isn’t the bacteria alone which can cause Alzheimer’s, but rather that the presence of these bacteria increases the risk for developing the disease considerably and are also implicated in a speedier evolution of the disease. Thanks to the findings from the study, Mydel says new medications could be produced which would postpone the development of Alzheimer’s, which they are planning to test later this year.

Alzheimer’s is one of the more poorly understood diseases. Scientists believe that for a majority of people, Alzheimer’s is caused by a combination of genetic, lifestyle and environmental factors which affect the brain over time, however, the exact causes aren’t yet fully understood. What is known and agreed upon is that it is associated with brain proteins which fail to function normally, disrupting neurons in the brain and unleashing toxic radicals. When that happens, it causes damage to those neurons which lose connection to one another and eventually die.

Mydel says that it is important, if you have established gingivitis and have Alzheimer´s in your family, to go to your dentist regularly and clean your teeth properly.

Alzheimer’s is a chronic neurodegenerative disease which affects nearly 44 million people around the globe and is most common in Western Europe. According to the BrightFocus Foundation, someone develops dementia every three seconds. Early signs of the disease may be short-term memory loss, and as the disease progresses, a person with Alzheimer’s disease will develop severe memory impairment and lose the ability to carry out everyday tasks.

Another study published in the Journal of the American Heart Association this month found common oral pathogens in 79 percent of cerebral blood clots samples of 75 stroke patients. Previous studies by the team at Tampere University in Finland found the same sort of bacteria in patients who’ve suffered heart attackscoronary stenosescerebral aneurysms and venous or arterial thrombosis.

Turns out your teeth are pretty important, so take care of them.

Green tea and carrot compounds reverse Alzheimer’s symptoms in mice

Credit: Pixabay.

Billions have been spent on research that might lead to new drugs for treating Alzheimer’s, but while substantial progress has been made, there’s not much yet in the way of a cure. But one new study suggests that dieting may be an important factor for managing the neurodegenerative disease’s symptoms. According to the findings, chemical compounds typically found in green tea and carrots reversed Alzheimer’s-like symptoms in mice.

“You don’t have to wait 10 to 12 years for a designer drug to make it to market; you can make these dietary changes today,” said senior author Terrence Town, a professor of physiology and neuroscience at the University of Southern California. “I find that very encouraging.”

Town and colleagues focused on two compounds: EGCG ( epigallocatechin-3-gallate), one of the main ingredients of green tea, and FA (ferulic acid), commonly found in carrots, tomatoes, rice, wheat, and oats. The researchers randomly assigned 32 mice, which were genetically modified to have Alzheimer’s, to one of four groups, divided into an equal number of males and females. For three months, mice were given a combination of EGCG and FA, either EGCG or FA only, or a placebo — yes, rodents also have the placebo effect. Additionally, a group of healthy mice provided baseline performance for Alzheimer’s-free symptoms.

Before and after the three-month diet, the rodents were subjected to a barrage of tests that gauged their thinking and memory skills. One such test involves a Y-shape maze in order to assess a mouse’s spatial working memory, which is key to finding your way out of a building.

A healthy mouse will explore each arm of the Y maze in search of food or a way out. They will enter the three arms in sequence more often than by chance alone. But rodents with Alzheimer’s-like symptoms don’t do this as well because their spatial memory is impaired, making them more likely to explore the same arm twice.

“After three months, combination treatment completely restored spatial working memory and the Alzheimer’s mice performed just as well as the healthy comparison mice,” Town said.

Alzheimer’s disease is widely believed to be caused by the accumulation of beta-amyloid proteins which clump together to form plaques between neurons and disrupt cell function. Another physical characteristic of the Alzheimer’s diseased brain is the buildup of tau proteins, which tangle inside neurons, blocking their transport system. Town suspects that the compounds prevent bigger amyloid proteins from breaking up into smaller amyloid beta proteins that clog neurons. They may also reduce neuroinflammation and oxidative stress in the brain, both important aspects of Alzheimer’s pathology.

But while the study is exciting, its findings apply to mice and most such discoveries never translate into human treatments. Even so, green tea and carrots are harmless and there’s nothing to stop people from including them in their diet. In the future, Town wants to explore this combination treatment further.

The findings appeared in the Journal of Biological Chemistry.

Credit: Wikimedia Commons.

Scientists may have finally found out what causes Alzheimer’s — and it might actually be those bleeding gums

Gingivitis causes the gums to become red, swollen, bleed easily — and, according to a new study, it might also cause Alzheimer’s when it goes untreated for decades.

Credit: Wikimedia Commons.

Credit: Wikimedia Commons.

It sounds incredible that something so low key, albeit annoying, as gum disease might be responsible for such a debilitating disease like Alzheimer’s that literally clogs your brain. However, evidence from multiple research groups is converging towards this conclusion.

After a certain age, the human brain starts to shrink considerably but surprisingly, not too many neurons die in the process. In the Alzheimer’s diseased brain, however, many neurons stop functioning, lose connections with other neurons, and eventually die.

In the early stage, the damage is confined to the entorhinal cortex and hippocampus, two areas associated with memory, navigation, and perception of time. This sort of degeneration leads to memory loss and disorientation associated with the condition — though it has to be noted that Alzheimer’s starts damaging brain cells well before the first symptoms kick in.

Alzheimer’s disease is widely believed to be caused by the accumulation of beta-amyloid proteins which clump together to form plaques between neurons and disrupt cell function. Another physical characteristic of the Alzheimer’s diseased brain is the buildup of tau proteins, which tangle inside neurons, blocking their transport system.

Could these protein plaques be simply byproducts of the brain’s defense mechanisms in the face of the real Alzheimer’s causing germ? Gum disease-causing bacteria such as Porphyromonas gingivalis (abbreviated Pg) have been found in the brains of people who had Alzheimer’s. What’s more, autopsies have shown that protein plaques can appear in people who had no Alzheimer’s disease.

Gum disease, which affects a third of all people, has been identified as one of the main risk factors for Alzheimer’s. Previously, researchers have shown that P. gingivalis causes inflammation in brain areas known to be heavily hit by Alzheimer’s, causing neural damage and amyloid plaques in healthy mice. And when mice that had been genetically engineered to have Alzheimer’s were infected with gum disease, their dementia symptoms worsen.

Now, researchers at Cortexyme, an American pharmaceutical corporation who has invested heavily in gum disease research, add even more weight to the gum disease-Alzheimer’s association.

“Infectious agents have been implicated in the development and progression of Alzheimer’s disease before, but the evidence of causation hasn’t been convincing,” said Stephen Dominy, M.D., Cortexyme co-founder and lead author on the paper. “Now, for the first time, we have solid evidence connecting the intracellular, Gram-negative pathogen, Pg, and Alzheimer’s pathogenesis while also demonstrating the potential for a class of small molecule therapies to change the trajectory of disease.”

In the new study, researchers examined the brains of 54 deceased individuals who had Alzheimer’s. They found toxins called gingipains produced by P. gingivalis in 96% of the samples and the bacterium itself in three samples. The most toxic enzymes were found in those with the worst cognitive decline — these samples also had more amyloid and tau protein accumulations.

The team also infected mice with gum disease, finding that the rodents acquired brain infection, along with tau and amyloid build up in regions normally affected by Alzheimer’s. When researchers exposed the mice to a substance previously developed by Cortexyme that blocks the production of gum disease-related toxins, infection was reduced and protein plaque accumulation stopped. Some damaged neurons even recovered.

Antibiotics also worked similarly well, but less effectively. Moreover, the bacteria eventually developed resistance but did not resist the gingipain blockers.

The authors of the new study published in Science Advances propose that Alzheimer’s develops when gingipains accumulate fast enough to cause a patient to show symptoms. Cortexyme’s gingipain blockers have passed initial safety tests and the company plans on launching a clinical trial soon that will investigate the drug’s effects on cognition. New Scientist reports that elsewhere, Australian researchers are working on a vaccine for P. gingivalis — if this vaccine prevents gum disease and Alzheimer’s at the same time, millions of people could be saved.

“We know diseases like Alzheimer’s are complex and have several different causes, but strong genetic evidence indicates that factors other than bacterial infections are central to the development of Alzheimer’s, so these new findings need to be taken in the context of this existing research,” Dr. David Reynolds, Chief Scientific Officer from Alzheimer’s Research UK, said in a statement. 

“Maintaining good dental health is an important part of a healthy lifestyle, and while we don’t yet fully know the extent to which it can affect our dementia risk, the presence of a single type of bacteria is extremely unlikely to be the only cause of the condition.

“Drugs targeting the bacteria’s toxic proteins have so far only shown benefit in mice, yet with no new dementia treatments in over 15 years it’s important that we test as many approaches as possible to tackle diseases like Alzheimer’s. It’s important we carefully assess all new potential treatments, and this drug is currently in an early phase clinical trial to establish if it is safe for people. We will have to see the outcome of this ongoing trial before we know more about its potential as a treatment for Alzheimer’s.”

Artificial Intelligence detects Alzheimer’s six years before human diagnosis

The algorithm is surprisingly good at spotting changes associated with Alzheimer’s disease, giving patients crucial time to intervene with treatment.

A PET scan of the brain of a person with Alzheimer’s disease. Image credits: National Institute on Aging.

As with many other conditions, early detection is crucial in Alzheimer’s. The problem, however, is that the symptoms aren’t usually clear — and by the time a diagnosis is done, most treatments lose efficacy. Although there is no direct treatment for Alzheimer’s, there are several treatments that can help stem the progress of the condition. Having a way to diagnose it sooner could make a huge difference in dealing with the disease.

“One of the difficulties with Alzheimer’s disease is that by the time all the clinical symptoms manifest and we can make a definitive diagnosis, too many neurons have died, making it essentially irreversible,” says Jae Ho Sohn, MD, MS, a resident in the Department of Radiology and Biomedical Imaging at UC San Francisco.

This is where the new AI comes in. Sohn and colleagues combined neuroimaging with machine learning, “training” the algorithm to analyze PET scans and look for Alzheimer’s-related patterns. They first fed it images from the Alzheimer’s Disease Neuroimaging Initiative (ADNI), a massive public dataset of PET scans from patients who were eventually diagnosed with either Alzheimer’s disease, mild cognitive impairment or no disorder.

The brain of a person with Alzheimer’s (left) compared with the brain of a person without the disease. Image credits: UCSF.

“This is an ideal application of deep learning because it is particularly strong at finding very subtle but diffuse processes. Human radiologists are really strong at identifying tiny focal finding like a brain tumor, but we struggle at detecting more slow, global changes,” says Sohn. “Given the strength of deep learning in this type of application, especially compared to humans, it seemed like a natural application.”

After 1,921 training scans, they fed it another 188 images — also from the same database, but not previously presented to the AI. An additional set of 40 scans from patients who had presented to the UCSF Memory and Aging Center with possible cognitive impairment. The AI passed with flying colors.

First of all, it was able to successfully identify 92% of patients who developed Alzheimer’s disease in the first test set and 98% in the second test set. Even more impressively, on average, it made the predictions 75.8 months (over 6 years) before the patient received the official diagnosis.

An algorithm of this type could be a very useful predictive tool for Alzheimer’s treatment. Of course, it will still be a while before the method can be clinically applied, but researchers are optimistic. Sohn wants to test the algorithm. But with additional validation and calibration in a larger setting, the device can be used, researchers say.

“I believe this algorithm has the strong potential to be clinically relevant,” Sohn concludes. The study has been published in Radiology.

Diabetes drugs may have protective effects against Alzheimer’s

Researchers analyzed brain tissue sourced from people who had both diabetes and Alzheimer’s. The findings suggest that some anti-diabetes drugs that these people used offered protection that kept the neurodegenerative disease from progressing as rapidly as it would have otherwise.

Credit: Pixabay.

Many elderly people with diabetes have brain changes that are hallmarks of Alzheimer’s. Previous studies have suggested that there is a link between the risk of cognitive impairment, dementia, and type 2 diabetes, and there is evidence that an insulin receptor pathway in the brain is associated with Alzheimer’s pathologies, though the mechanism remains unknown.

A while ago, researchers at the Icahn School of Medicine at Mount Sinai in New York led by Vahram Haroutunian — a professor of psychiatry and neuroscience — found that the brains of people with Alzheimer’s who had also undergone treatment for diabetes (insulin or medicine) had reduced brain pathologies.

This time, Haroutunian and colleagues wanted to dive deeper, at the molecular level, to identify the specific pathways that may explain the association between diabetes and Alzheimer’s.

Using a technique that they designed, the team isolated brain capillaries from the brain tissues of 34 individuals who had both Alzheimer’s and type 2 diabetes, and who were treated for both. The researchers specifically focused on endothelial cells that line the inside of blood vessels and form an interface between circulating blood and the rest of the vessel wall.

The team compared the tissues to those of 30 people who had had Alzheimer’s but not diabetes, as well as 19 control subjects that had neither of the two diseases.

The findings suggest that individuals who were treated for both diseases had half as many markers for Alzheimer’s-related molecular changes in the brain’s capillary cells compared to those that only had Alzheimer’s. What’s more, the majority of molecular changes in RNA markers present in Alzheimer’s disease were not encountered in the study group that took medication for diabetes.

“The results of this study are important because they give us new insights for the treatment of Alzheimer’s disease,” said the study’s senior author, Vahram Haroutunian.

“Most modern Alzheimer’s treatments target amyloid plaques and haven’t succeeded in effectively treating the disease,” said Dr. Haroutunian. “Insulin and diabetes medications such as metformin are FDA approved and safely administered to millions of people and appear to have a beneficial effect on people with Alzheimer’s. This opens opportunities to conduct research trials on people using similar drugs or on drugs that have similar effects on the brains’ biological pathways and cell types identified in this study.”

The findings appeared in the journal PLOS One.

Bill Gates and other philantropists invest $30 million to boost early Alzheimer’s detection

Along with Estée Lauder chairman emeritus Leonard Lauder, Bill Gates announced a new $30m award to encourage the development of new tests for early detection of Alzheimer’s disease. The money will be awarded over three years.

PET scan of a human brain with Alzheimer’s. Image credits: NIH.

In 2013, as many as 5 million Americans were living with Alzheimer’s disease and the CDC estimates that by 2050, the number will grow to 16 million. Elsewhere in the world, figures are similar, with 9.9 million new cases of dementia each year worldwide, implying one new case every 3.2 seconds.

Age is the best-known risk factor for the disease, although family history and lifestyle also play significant roles in the development of the disease. Other aspects, such as education have been linked to a reduction in Alzheimer’s cases, but that link is still being investigated. At any rate, early detection is critical to the management of the disease — and this is where Bill Gates steps in.

Gates, who recently announced that his father suffers from Alzheimer’s, has already invested $100 million towards stopping the disease, and has been particularly interested in understanding the onset and early stages of Alzheimer’s

“One of the things we’re trying to figure out is, when does the Alzheimer’s really get started?” he told NBC’s Maria Shriver in January. “When would you need to treat somebody to completely avoid them getting Alzheimer’s?”

Gates and Lauder provided seed money for the diagnostics collaboration through the Alzheimer’s Drug Discovery Foundation (ADDF), which was founded by Lauder. They’re not the only two investors in this fund — the Dolby family and the Charles and Helen Schwab Foundation will also contribute.

The funding will be available to scientists and clinicians globally, as long as they work in academic settings, charities, or biotechnology companies. The program, dubbed the Diagnostics Accelerator, will also invest into riskier projects, which may not have an immediate commercial return, and are therefore less likely to receive other types of funding.

Currently, Alzheimer’s diagnosis is a long and painstaking process, involving several cognitive tests, followed by a brain scan or a spinal tap, which are used to determine whether the patient is suffering from Alzheimer’s or another type of dementia. The process is not only lengthy, but also expensive, and in the case of a spinal tap, quite painful.

Additionally, patients don’t typically get tested for the disease until they start showing cognitive decline — and by that point, much of the damage has already been done. In a recent blog post, Gates writes:

“Research suggests Alzheimer’s starts damaging the brain more than a decade before symptoms start showing. That’s probably when we need to start treating people to have the best shot at an effective drug.”

Gates envisions a world where having an Alzheimer’s test is as simple as “getting your blood tested during your yearly physical.”

Research suggests that future isn’t that far off, and Diagnostics Accelerator moves us one step closer,” Gates concludes.


Scientists reverse damage by key gene involved in Alzheimer’s Disease

Alzheimer’s Disease (AD) is a debilitating neurogenerative disease for which there is no cure. Among the several risk factors for AD, a certain gene called APOE4 seems to play a major role. Now, scientists have reported correcting this gene variant, erasing its harmful effects.


Credit: Pixabay.

The apolipoprotein (APOE) gene plays a very complex role in the development of Alzheimer’s. This gene comes in three variants: APOE2, E3, and E4. Everybody carries two of these three variants, with the most common variant being APOE3. Some people — about 15 percent of the general population — have APOE4, which increases the risk of AD by up to a factor of three. Those extremely unfortunate enough to have two copies of the gene are 12 times likelier to develop the neurodegenerative disorder.

In a new study, researchers at the Gladstone Institutes in San Francisco, CA, set out to find out what makes the E4 variant so dangerous.

The main role of the APOE gene is to code instructions for the production of a certain protein with the same name. When this protein is combined with fats, lipoproteins emerge, which help to transport and regulate levels of cholesterol throughout the bloodstream. The APOE proteins created by the E3 and E4 variants are very similar, with the two differing very little at only one point. However, even such a tiny difference could have important effects on the human body. For instance, the E4 variant may be causing APOE3 to lose some of its functions or it could be the case that APOE4 has some toxic effects.

In order to investigate how the variants might influence AD development, the researchers modeled the disease in human cells, monitoring the effects of APOE4 on human brain cells for the very first time. This, in and of itself, was already a huge step forward in AD research because more often than not work on animal models, such as experimental drugs, is not transferable to humans.

Can Alzheimer’s be reversed?

Researchers collected skin cells from Alzheimer’s patients with two APOE4 genes, as well as some from people with two APOE3 genes who didn’t have Alzheimer’s. Using stem cell technology, the skin cells were turned into induced pluripotent stem cells, which were, in turn, converted into human brain cells. When the neurons from the APOE3 and APOE4 donors were compared, the researchers found that the latter didn’t function as well as they should. Specifically, the proteins break down into the neurons, leading to higher levels of tau phosphorylation a marker for AD. Intriguingly, the “APOE4 increased [amyloid-beta] production in human, but not in mouse, neurons,” once again highlighting the potentially huge discrepancy in results between animal and human studies.

“There’s an important species difference in the effect of apoE4 on amyloid beta,” said Chengzhong Wang, first author of the new study published in Nature Medicine. “Increased amyloid beta production is not seen in mouse neurons and could potentially explain some of the discrepancies between mice and humans regarding drug efficacy. This will be very important information for future drug development.”

The authors of the new study conclude that the APOE4 protein has a “pathogenic conformation” — in other words, the protein’s structure has an abnormal form that prevents it from functioning properly. And it is this abnormality that leads to disease-causing complications.

The good news is that the researchers were able to reverse the damage by applying a class of compounds that turn APOE4 into APOE3. It’s thus reasonable to assume that it may be possible to treat brain cells with such structure-correcting molecules to restore neuron function. This may actually open up an effective treatment route to reverse the signs of Alzheimer’s, which today is impossible to do. In the future, the team plans on testing such a hypothesis in human patients.

“Treatment of APOE4-expressing neurons with a small-molecule structure corrector ameliorated the detrimental effects, thus showing that correcting the pathogenic conformation of APOE4 is a viable therapeutic approach for APOE4-related [Alzheimer’s disease],” the authors concluded.

Poor sleep linked to increased risk of Alzheimer’s disease

Researchers have discovered that daytime sleepiness might cause brain build-ups leading to Alzheimer’s disease (AD).

Via Pixabay/gracic

Elderly people feeling drowsy during the day due to poor sleep or waking up in the night had a greater build-up in their brain of amyloid plaques which consume the brain, kill cells, and eventually lead to total memory loss. And this makes sense: recent studies have shown that while the brain sleeps, it clears away deposits of amyloid.

Even though previous research showed a correlation between sleepiness and AD, scientists wondered if the accumulation of amyloid plaques in the patients’ brains caused sleep problems or if it was the other way around.

Now, a team led by Mayo Clinic’s Prashanthi Vemuri has cast light on the subject: sleep itself seems to be causing the plaque accumulation that triggers the neurodegenerative disease.

“This study is the first in humans to demonstrate a predictive association between a measure of sleep disturbance at baseline and change in an AD [Alzheimer’s disease] biomarker across multiple points,” Joseph R. Winer and Bryce A. Mander, of the University of California, wrote in an editorial published with the study in the Journal of the American Medical Association.

The research team studied 283 people aged 70 or older without dementia from the center’s Study of Aging. Each participant completed surveys that assessed their general sleepiness and had at least two consecutive imaging scans of their brains from 2009 to 2016. The scans monitored the difference in amyloid plaque quantity between two scans in different regions of the brain.

Researchers discovered that 63 participants (22.3%) had excessive daytime sleepiness, and this was associated with increased amyloid plaque accumulation in susceptible regions of the brain.

“We found that daytime sleepiness was causing more deposition of amyloid in people who are already amyloid positive, so it was influencing the rate of deposition over time,” Dr. Vermuri said.

Although the study seems to establish causation between sleep patterns and amyloid accumulation, the team still has no definitive answer to why and how sleep has this effect.

However, experts consider this study a breakthrough, believing the findings underline the importance of good sleep for preserving brain health.

“This study and others present evidence that poor sleep quality may be an early warning sign of AD-related processes,” Winer and Mander wrote. “Although a better understanding of the role of sleep in the AD cascade could soon lead to effective sleep-based therapies, at present, maintaining healthy sleep and treating clinical sleep disorders must be a current priority for mental health in older adults.:

Bill Gates invests $100 million to study and defeat Alzheimer’s

Say what you want about Gates as a businessman but as a philanthropist, he’s definitely putting his money where his mouth is. His latest enterprise is fighting Alzheimer’s disease, which affects 30 million people every year and kills almost 2 million.

A health revolution

Despite what you may see on the news, this is the best time to be alive. This isn’t saying that everything is peachy in the world — quite the opposite can be said in many areas of the planet — but it is, on average, better than at any point in human history. Thanks to continuous advancements in science, we’re living more than ever. In the developed world, at least, people routinely live to be 80 or even 90 years old. In other words, we’ve pretty much figured out how to make people live longer, though the practices aren’t yet implemented in most parts of the world. But now, it’s time for a new revolution: it’s not only about making people live longer, but it’s more about making sure that they make the most out of those extra years.

“In every part of the world, people are living longer than they used to,” Gates writes on his blog. “Thanks to scientific advancements, fewer people die young from heart disease, cancer, and infectious diseases. It’s no longer unusual for a person to live well into their 80s and beyond. My dad will celebrate his 92nd birthday in a couple weeks, a milestone that was practically unimaginable when he was born.”

“This fact—that people are living longer than ever before—should always be a wonderful thing. But what happens when it’s not?”

Gates was specifically referring to Alzheimer’s. The disease, which causes 60% to 70% of cases of dementia, devastates both those who have it and their loved ones. The most common early symptom is difficulty in remembering recent events, but as the disease progresses, symptoms become much stronger and harder to manage.

The causes of Alzheimer’s are poorly understood, but scientists have seen that the disease is tightly connected to aging. The damage that the disease does is also very difficult to quantify. However, the financial cost is easier to calculate. As Gates explains, Americans will spend $259 billion caring for those with Alzheimer’s and other dementias in 2017. Unless unforeseen advancements take place in future years, that figure will continue to grow.

“I first became interested in Alzheimer’s because of its costs—both emotional and economic—to families and healthcare systems. The financial burden of the disease is much easier to quantify. A person with Alzheimer’s or another form of dementia spends five times more every year out-of-pocket on healthcare than a senior without a neurodegenerative condition. Unlike those with many chronic diseases, people with Alzheimer’s incur long-term care costs as well as direct medical expenses. If you get the disease in your 60s or 70s, you might require expensive care for decades.”

Investing in a healthier future

In the case of Alzheimer’s, just like in most medical problems, hefty investments can not only improve the quality of life for people, but they can also save a lot of money. Gates believes that by investing $100 million, he will be saving mankind much more than that in the long run, in addition to making a positive impact for millions of people. So he’s investing $50 million in start-up ventures working in Alzheimer’s research, and another $50 million in the Dementia Discovery Fund — a fund that brings together NGOs, governments, and industries to provide much-needed investment in innovative therapies and treatment avenues for Alzheimer’s. The main objectives of this investment are:

  • Understanding how Alzheimer’s emerges and unfolds. The brain is a complex and complicated organ, every disease that affects it is bound to be complex itself.
  • Diagnosing Alzheimer’s sooner. There is no direct way to diagnose Alzheimer’s — except an autopsy. We need to better identify this disease if we want to treat it.
  • Finding more treatment approaches. Many drugs to treat Alzheimer’s exist, but they generally follow similar avenues. We need to diversify our approach, Gates says.
  • Making it easier for people to get involved in clinical trials. There’s a lot of research going on in the field, but it can sometimes take years to enroll patients for studies.
  • Using data in a better way. Every time a study is carried out, lots and lots of information are gathered, but sometimes, this data isn’t accessible or compiled for others to use.

“By improving in each of these areas, I think we can develop an intervention that drastically reduces the impact of Alzheimer’s. There are plenty of reasons to be optimistic about our chances: our understanding of the brain and the disease is advancing a great deal. We’re already making progress—but we need to do more,” Gates concludes.