Tag Archives: alzheimer’s disease

Scientists find Viagra may treat Alzheimer’s disease

Credit: Pixabay.

Sildenafil, a drug most typically used to address erectile dysfunction, may surprisingly work wonders in staving off Alzheimer’s disease, the most common cause of dementia across the world. At the moment there is no proper treatment for Alzheimer’s, an incurable disease that is highly debilitating and whose burden of society is increasing every year with an aging population.

Two pathways, a single drug

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.  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.

“Many drug discovery projects focused on anti-amyloid pathways failed in the past two decades. In our project, we test a novel hypothesis of dual targeting both amyloid and Tau pathways at the same time compared to the traditional drug discovery approach targeting amyloid and Tau pathways alone. As Alzheimer’s disease (AD) is a complex disease caused by many factors, multi-target drugs or combination therapy that target multiple disease pathways may offer better clinical benefits for complex diseases, like AD,” Dr. Feixiong Cheng of Cleveland Clinic’s Genomic Medicine Institute and lead author of the new study told ZME Science.

Cheng and colleagues set out to find new or existing drugs whose biological pathways may intersect with Alzheimer’s. This was a challenging task that resulted in a lot of dead ends as more than 99% of proposed drugs for Alzheimer’s disease have turned out to be hugely disappointing failures in clinical trials.

So the researchers decided to get back to the drawing board and try something different: target both amyloid and Tau pathways at the same time. They went to work and designed a computational model that mapped out a large network of over 350,000 human protein-protein interactions. This huge gene-mapping network allowed the researchers to single out over 1,600 FDA-approved drugs that could target both amyloid and tau, and thus potentially treat Alzheimer’s disease.

The best drug candidate was sildenafil, a drug famous for treating erectile dysfunction under the brand name Viagra and pulmonary hypertension under the brand name Revatio. Previously, sildenafil has been associated with improvements in cognition and memory in preclinical models.

In order to see what kind of effect sildenafil might have on Alzheimer’s, the researchers closely looked at insurance claims data from over seven million Americans. This analysis revealed that sildenafil prescriptions were associated with a 69% reduction in the risk of AD diagnosis after 6 years of follow-up. 

Of particular note is that sildenafil was most likely to reduce the incidence of Alzheimer’s in individuals with coronary artery disease, hypertension, and type 2 diabetes, all of which are comorbidities significantly associated with the neurodegenerative disease.

Back in the lab, the researchers used stem cells to grow  Alzheimer’s patient-derived brain cells. When sildenafil was introduced in the tissue, the brain cells’ rate of growth increased while the hyperphosphorylation of tau proteins (a hallmark that leads to neurofibrillary tangles) decreased.

All of these findings in combination point towards sildenafil as a worthy drug candidate for Alzheimer’s, which is why the researchers are now planning a phase II randomized clinical trial to confirm the drug’s clinical benefits for patients with the disease. And despite sildenafil’s notorious reputation, embarrassing moments are highly unlikely.

“We don’t think daily erections are a major side effect of sildenafil as we will use sildenafil in elderly individuals and we can control this issue by adjusting dosage and other factors. We are planning a phase II trial to test the clinical benefits of sildenafil in early of AD patients in the next step. We will answer dosage issues in our future RCT (clinical trial),” Cheng said.

“AD is a complex disease and we have to use personalized treatment (precision medicine) and drug combination therapy strategies to prevent and treat AD in the future. In our project, we found that dual-targeting both Tau and amyloid pathways may offer better clinical benefits compared to the traditional approach targeting Tau and amyloid pathways alone. There are other types of endophenotypes, such as inflammatory pathways as well, and we are working on combination therapy design by combining Tau and amyloid endophenotype with anti-inflammatory therapies in the next step as well,” he added.

The findings were reported in the journal Nature Aging

New neurons are formed in the brain well into old age — but this stops in Alzheimer’s

The magic happens in the hippocampus.

Image credits: Gerry Shaw.

The majority of our neurons are already in place by the time we are born, although some are still produced during childhood. Traditionally, it was thought that no new neurons are produced during adulthood, but researches are still arguing whether this is truly the case.

Neurogenesis, the production of new neurons, has remained a controversial topic. A recent study found that even if new neurons are produced into adulthood, this process happens early in adulthood, and is very limited. Other studies have claimed that neurogenesis doesn’t happen at all, while some teams have reported evidence of new neurons being formed. The situation is still murky, but a new study tries to clear the waters, reporting that neurons are formed well into old age.

According to a paper published in Nature Medicine, new neurons continuously develop in the healthy human brain up to the ninth decade of life — at least in the hippocampus. Maria Llorens-Martin and colleagues from the Universidad Autónoma de Madrid analyzed tissue samples from 58 human participants.

They found that while neurogenesis can decline with old age, it is still present across the lifespan in the hippocampus, particularly in an area called the dentate gyrus, a region associated with the formation of new episodic memories and the spontaneous exploration of novel environments.

They also find that this process decreases sharply in people suffering from Alzheimer’s.

“By combining human brain samples obtained under tightly controlled conditions and state-of-the-art tissue processing methods, we identified thousands of immature neurons in the dentate gyrus of neurologically healthy human subjects up to the ninth decade of life. These neurons exhibited variable degrees of maturation along differentiation stages. In sharp contrast, the number and maturation of these neurons declined as AD advanced.”

So not only does the study provide new insight on neurogenesis, but it also highlights a mechanism associated with Alzheimer’s.

“The hippocampus is one of the most affected areas in Alzheimer’s disease,” researchers write in the paper. “Moreover, this structure hosts one of the most unique phenomena of the adult mammalian brain, namely, the addition of new neurons throughout life.”

As for the discrepancies between this study and previous results, researchers say it’s owed to methodological differences. Having high-quality samples and processing them properly and quickly is vital, they argue — otherwise, the evidence of neurogenesis can be destroyed. Factors such as tissue fixation techniques or delays in the time between tissue acquisition and processing can alter the results, they explain.

“Our data demonstrate that the prolonged or uncontrolled fixation conditions to which human samples are typically exposed in brain banks worldwide lead to a sharp reduction in the number of [neurons] detected in the adult dentate gyrus,” the paper concludes.

The study “Adult hippocampal neurogenesis is abundant in neurologically healthy subjects and drops sharply in patients with Alzheimer’s disease” has been published in Nature Medicine.

 

Eye scan might detect Alzheimer’s disease

Tiny blood vessels in the back of the eye, which are thinner than a human hair, may signal the presence of Alzheimer’s disease. A new eye scan test, developed by researchers at the Duke Eye Center, suggests this connection can be exploited to detect the neurodegenerative disease before symptoms become too severe to respond to treatment.

Credit: Pixabay.

Diagnosing Alzheimer’s disease is tricky. Symptoms progress slowly over several years and can be easily confused with other conditions that may initially be attributed to old age. By the time it’s obvious that a person has Alzheimer’s it’s already too late, as the disease has already eaten away too many brain cells.

There is no cure for Alzheimer’s but research suggest that it is possible to delay its onset by several years if the condition is diagnosed early on. Some techniques, such as brain scans or spinal taps, can theoretically detect Alzheimer’s fairly early, however, they can’t be scaled to screen the millions of people who are vulnerable to the disease. An early diagnosis also gives patients and their families some valuable time to plan for the future.

This is why this latest study is so exciting — it suggests that it’s possible to detect Alzheimer’s simply by imaging the back of the eye. The non-invasive imaging technique, called optical coherence tomography angiography (OCTA), is based on the idea that since the retina is an extension of the brain, the two also share similar features.

In order to investigate whether damage to the retina may mirror changes in the brain’s blood vessels, researchers compared 70 eyes of 39 Alzheimer’s patients with 72 eyes of 37 people with mild cognitive impairment, as well as 254 eyes of 133 cognitively healthy people. According to the results, the Alzheimer’s group had lost some of their retinal blood vessels in the back of the eye. A specific layer of the retina was also thinner in this group compared to people with mild cognitive impairment or healthy individuals.

In the future, this technique could prove to be a quick, noninvasive, and inexpensive way to detect Alzheimer’s at the earliest stages.

“Early diagnosis of Alzheimer’s disease is a huge unmet need,” Sharon Fekrat, M.D., Professor of Ophthalmology at Duke, said in a statement. “It’s not possible for current techniques like a brain scan or lumbar puncture (spinal tap) to screen the number of patients with this disease. It is possible that these changes in blood vessel density in the retina may mirror what’s going on in the tiny blood vessels in the brain. Our work is not done. If we can detect these blood vessel changes in the retina before any changes in cognition, that would be a game changer.”

The findings appeared in the journal Ophthalmology.

Scientists reverse leading cause of late-onset Alzheimer’s, opening door for vaccine that prevents the disease

Credit: Pixabay.

A team of researchers at the University of Texas Southwestern Medical Center may have found a way to prevent Alzheimer’s disease from clogging brain tissue. Their novel approach could be turned into a drug or vaccine that would prevent the debilitating disease in 50 to 80% of at-risk adults.

Alzheimer’s is the leading cause of dementia. The neurodegenerative disease affects cognitive and thinking abilities, making day-to-day life incredibly challenging in its most advanced stages.

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 even before the first symptoms kick in.

Later on, the disease starts to hit the cerebral cortex responsible for language, reasoning, and social behavior, from where it eventually spreads to other brain areas.

Research has shown that individuals with Alzheimer’s disease accumulate 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 the cells’ transport system.

Currently, there is no available cure for Alzheimer’s disease. Most research efforts are focused on findings ways to halt the progress of the disease and reduce its symptoms. However, molecular biologist Joachim Herz and colleagues at UT Southwestern have embarked on a different route: instead of looking for ways to stop the spread of amyloid and tau accumulation when the process has already set in, the researchers are looking to prevent the buildup from happening in the first place. In other words, they want to prevent the disease rather than treat it.

There are three major forms of Apolipoprotein E (ApoE) proteins that play a vital role in the brain tissue repair by carrying lipids and cholesterol around the brain. However, individuals who carry ApoE4 are up to 10 times more likely to get Alzheimer’s than those with the ApoE2 and ApoE3 forms.

Herz and colleagues claim that ApoE4 causes “traffic jams” inside neuron cells, thereby leading to inefficient recycling of intracellular endosomal transport vesicles. Their research on mice found that lowering the pH of these endosomes (making them more acidic) cleared the traffic jams. Specifically, the ApoE4-induced blockages were reversed by inhibiting the NHE6 protein, which is responsible for making endosomal vesicles less acidic.

“Our approach in this study was to stop the overall degeneration process earlier; that is, before the formation of these aggregates [i.e. amyloid and tau protein],” Dr. Herz said in a statement.

The findings provide a new therapeutic pathway that could prevent Alzheimer’s in 50% to 80% of at-risk adults. A vaccine or drug that selectively blocks NHE6 could be administered before age 40, providing a lifetime of Alzheimer’s protection. Developing such tailor-made molecules is the next step for the UT Southwestern researchers.

“The beauty of NHE inhibitors is that these are small molecules that can be produced inexpensively and thus made widely available, in contrast to the more elaborate antibody-based therapies that are currently being evaluated in clinical trials. A simple pill could someday neutralize the risk of late-onset Alzheimer’s disease just as readily available statins are able to reduce the risk of cardiovascular disease,” Dr. Herz said.

The findings were reported in the journal eLife.

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.

dementia vs alzheimer's

What’s the difference between Alzheimer’s and Dementia?

dementia vs alzheimer's

Credit: Pixabay

There is often confusion and misunderstanding surrounding the terms Alzheimer’s disease and dementia. Though the two are certainly related there are significant differences that people should know.

Main differences between Alzheimer’s disease and dementia

  • Dementia is a syndrome while Alzheimer’s is a disease that causes dementia symptoms akin to HIV vs AIDS. You may also hear dementia described as a condition.
  • Alzheimer’s disease is the best known of these diseases and the most common cause of dementia. There are, however, over 200 types of dementia besides Alzheimer’s.

What is dementia

Dementia represents “a general term for a decline in mental ability severe enough to interfere with daily life,” according to the American non-profit Alzheimer’s Association. A wide set of symptoms can apply, but there are certain smoking guns, like poor judgment or memory loss. Simplifying things, a disease like Alzheimer’s damages the brain and too much damage will impair its ability to function. This translates to observable symptoms that tend to develop hand in hand as the physiological damage worsens in the brain. It’s this set of symptoms that we refer to as “dementia.”

Alzheimer’s is far from being the sole culprit, though. While Alzheimer’s accounts for 60-70 percent of dementia cases, other causes include Vascular dementia, Parkinson’s disease, dementia with Lewy Bodies and Frontotemporal dementia.

There are around 47.5 million people around the world living with dementia according to the World Health Organization. 

Dementia symptoms

The onset of early dementia can be difficult to spot. At first, people can have simple episodes of forgetfulness, which can happen to anyone. These bouts of trouble remembering people and events can persist for a long time though and that’s when it starts becoming a problem. Steadily, people with dementia will find it increasingly difficult to keep track of time or navigate familiar settings.

Confusion and forgetfulness become more prevalent, as well. Ultimately, in the more advanced stage of dementia, most patients become unable to care for themselves.

During the early stages of dementia, there can be some clear differences in symptoms based on the underlying disease. In patients with Lewy Bodies, the second most common cause of dementia, early symptoms are more about lowered attention span, visual hallucinations, and fluctuations in bouts of lucidity and confusion.

Diagnosing the underlying disease, however, becomes challenging as it advances and affects more parts of the brain. These differences become so subtle that doctors can sometimes misdiagnose. Screening methods include blood tests, mental status evaluation and, as of more recently, brain scans. Dementia-causing diseases, such as Alzheimer’s, can only be diagnosed with complete accuracy after death by examining the brain tissue for signs of plaques and tangles.

What is Alzheimer’s disease

Brain scans showing the differing distribution of amyloid plaques and tau tangles in patients with Alzheimer's disease. Credit: University of California.

Brain scans showing the differing distribution of amyloid plaques and tau tangles in patients with Alzheimer’s disease. Credit: University of California.

Alzheimer’s disease is a brain disorder that affects memory and thinking skills. Symptoms typically develop slowly but progressively get worse over time. Eventually, the disease can disrupt the ability to carry out even the simplest of tasks. Alzheimer’s impact is irreversible. There is no cure.

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

In the early stage, the damage is confined to the entorhinal cortex and hippocampus. The first functions as a hub in a widespread network for memory and navigation while the latter is one of the most important brain components where long-term memories are stored. This sort of degeneration leads to the 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.

Later, the disease starts to hit the cerebral cortex responsible for language, reasoning, and social behavior, from where it eventually spreads to other brain areas.

Decades of research show that Alzheimer’s causes molecular and cellular changes in the brain. These are evident in tissue samples collected from deceased patients.

One common physical characteristic in brains affected by the condition is the accumulation of beta-amyloid proteins which clump together to form plaques between neurons and disrupt cell function. There are many forms of beta-amyloid proteins and researchers are still busy unraveling the many threads.

Another notable characteristic is abnormal accumulations of a protein called tau that builds up inside neurons. In a healthy brain, tau normally binds to and stabilizes microtubules, which are internal structures that support the neuron and guide nutrients and molecules from the cell body to the axon and dendrites. Abnormal chemical changes inside the Alzheimer’s brain, however, cause tau to detach from microtubules and stick to other tau molecules. Eventually, these tangle inside the cell blocking the neuron’s transport system.

Alzheimer’s is more common as people grow older but it’s definitely not a normal part of aging. What’s more, you don’t necessarily have to reach a ripe old age to be at risk of Alzheimer’s. Approximately 200,000 Americans under the age of 65 develop Alzheimer’s disease (also known as early-onset Alzheimer’s). In fact, one study found Alzheimer’s can affect people in their 20s.

Those with Alzheimer’s live an average of eight years after their symptoms become noticeable to others, but survival can range from four to 20 years, depending on age and other health conditions.

While there is currently no cure, there are available treatments that can slow the worsening of the dementia symptoms. Scientists are relentlessly pursuing, however, novel treatments and methods to delay its onset and prevent it from developing.

Alzheimer’s symptoms

Doctors diagnose Alzheimer’s using a barrage of medical tests, which include:

  • blood tests
  • mental health evaluations
  • brain scans (only in some cases)

Alzheimer's severely shrinks brain volume, a phenomenon called brain atrophy. Credit: Wikimedia Commons.

Alzheimer’s severely shrinks brain volume, a phenomenon called brain atrophy. Credit: Wikimedia Commons.

It’s normal to occasionally find it difficult to remember certain things or think slowly. Persistently feeling confused and serious memory loss may be signs of brain cell failure.

The most common early symptom of Alzheimer’s is failing to remember newly acquired information. As the disease progresses irremediably, more severe symptoms will crop out such as:

  • disorientation;
  • mood and behavior swings;
  • confusing events, time, and places;
  • trouble remembering names and faces;
  • unfounded suspicions about family, friends, and caregivers;
  • serious memory loss;
  • difficulty speaking, swallowing and walking.

What makes Alzheimer’s particularly stressing, especially for the patient’s family and caregivers, is that patients may not recognize they have a problem.

Alzheimer’s research and future outlook

Since there is no cure for Alzheimer’s, early diagnosis is critical in order to delay the onset of severe dementia symptoms.

Research is making good progress, though, and one day it might be possible to prevent Alzheimer’s altogether. In 2016, scientists at the Baylor College of Medicine, Texas Children’s Hospital, and Johns Hopkins University School of Medicine, inhibited an enzyme which consistently resulted in lower levels of tau in both human cells and fruit flies. Drugs designed to block this enzyme could thus prevent Alzheimer’s from settling in.

Even more remarkably, in 2015, researchers at Midwestern University in Downers Grove, IL, reported in the journal Neuroscience how an intravenous drug reversed the effects of Alzheimer’s in mice.

Neuroscientists Case Western Reserve University School of Medicine discovered that bexarotene, a skin cancer drug, astonishingly also appears to reverse cognitive and memory deficits, commonly associated with Alzheimer’s when tested on lab mice. The drug seems to clear amyloid proteins in the brain, whose build-up is closely related to Alzheimer’s progression. Mice inflicted with Alzheimer’s were given the drug, and all showed clear signs of cognitive recovery.

Other studies, though not as spectacular, provide helpful insight. For instance, one recent peer-reviewed paper found men who frequent saunas are less likely to be diagnosed with dementia later in life. Another correlative study found extra-virgin oil might protect your brain from Alzheimer’s and improves synapses. Olive oil reduces brain inflammation and activates the autophagy process, cleaning some of the intracellular debris and toxins in the process.

Alzheimer’s is still a devastating disease to this moment, unfortunately. Families and friends of patients can at least live with the comfort that countless dedicated professionals are working on ways to curb the disease. Maybe, one day, it’s Alzheimer’s and other dementia that will become a fading memory instead of people’s most precious moments.

Alzheimer’s disease connected to reduced pain perception

Alzheimer’s disease is a progressive form of dementia that causes problems in memory, thinking and behavior. After sufficient progression, those suffering from it can face extremely difficulty when trying to conduct even simple tasks. Now, a new study from researchers from Vanderbilt University in Nashville suggests that the disease might also hinder people’s ability to recognize when they are in pain.

Image credit Pixabay

Image credit Pixabay

The study spanned three years and examined two groups of adults aged 65 and older. One group consisted of patients with Alzheimer’s disease, while the other was a control group without dementia. Using a device to expose participants to various heat sensations, the researchers gathered self-reported pain levels from each individual and analyzed the results.

“We found that participants with Alzheimer’s disease required higher temperatures to report sensing warmth, mild pain and moderate pain than the other participants,” said Todd Monroe, an assistant professor at Vanderbilt’s School of Nursing and lead author of the study.

Interestingly, although the study found lessened pain recognition in those with Alzheimer’s disease, their pain tolerance remained the same as the control group.

“What we didn’t find was a difference between the two groups in reporting how unpleasant the sensations were at any level,” Monroe said. “While we found that their ability to detect pain was reduced, we found no evidence that people with Alzheimer’s disease are less distressed by pain nor that pain becomes less unpleasant as their disease worsens.”

The inability to detect pain can have a cascade of effects by allowing underlying health issues to go undetected and untreated, ultimately leading to serious problems in the body such as organ damage.

Since the researchers used participant reports to gauge pain levels, the neural mechanisms behind the changes in pain perception found in the study are still unclear. Further research is needed to better understand exactly how Alzheimer’s disease is connected to pain perception and how to help patients detect discomfort, especially when they begin to have difficulties with verbal communication

“As people age, the risk of developing pain increases, and as the population of older adults continues to grow, so will the number of people diagnosed with Alzheimer’s disease,” Monroe said. “We need to find ways to improve pain care in people with all forms of dementia and help alleviate unnecessary suffering in this highly vulnerable population.”

Journal Reference: Contact heat sensitivity and reports of unpleasantness in communicative people with mild to moderate cognitive impairment in Alzheimer’s disease: a cross-sectional study. 10 May 2016. 10.1186/s12916-016-0619-1

Scientists move closer to world’s first Alzheimer’s disease vaccine

A team of researchers from the United States and Australia has made a breakthrough in the creation of a vaccine that can target the abnormal beta-amyloid and tau proteins that are involved in the development of Alzheimer’s disease.

Image credit Pixabay

Image credit Pixabay

Each year, 7.5 million people develop Alzheimer’s and it is quickly becoming one of the biggest costs to healthcare systems worldwide. Despite ongoing research, scientists have yet to discover a cure for the disease. However, the recent findings published in Scientific Reports suggest that an effective vaccine might be on the horizon.

“If we are successful in pre-clinical trials, in three to five years we could be well on the way to one of the most important developments in recent medical history,” said Nikolai Petrovsky of the Flinders University School of Medicine and co-author of the study.

Petrovsky highlights the necessity of a vaccine by pointing to the increase in type 2 diabetes cases in the West, which fuels the rise in dementia, as well as our rapidly aging populations.

The team used a combination of anti-amyloid-beta and anti-tau vaccines and an adjuvant technology called Advax to create a vaccine that generates antibodies that effectively bind to the amyloid and tau molecules in brain tissue obtained from patients with Alzheimer’s disease. Thus far, the vaccine has not shown any negative effects on immune system response.

“This study suggests that we can immunize patients at the early stages of AD, or even healthy people at risk for AD, using our anti-amyloid-beta vaccine, and, if the disease progresses, then vaccinate with another anti-tau vaccine to increase effectiveness,” said Anahit Ghochikyan of the Institute of Molecular Medicine (IMM) Department of Molecular Immunology and co-author of the study.

As of now, the team is working on non-clinical safety-toxicology studies to ensure that the vaccine meets government safety standards. After these pre-clinical studies are completed, they plan to move on to human trials.

Journal Reference: Alzheimer’s disease AdvaxCpG- adjuvanted MultiTEP-based dual and single vaccines induce high-titer antibodies against various forms of tau and Aβ pathological molecules. 22 June 2016. 10.1038/srep28912

Peanut Butter Sniff Test Confirms Alzheimer’s

A lump of peanut butter and a ruler are sufficient to confirm an Alzheimer’s diagnosis, even in its early stages, researchers claim.

#ds314 - Yes. With a Spoon.

Credit: Sharon Drummond/Flickr

Jennifer Stamps, a graduate student in the McKnight Brain Institute Center for Smell and Taste and the University of Florida came up with the idea of using peanut butter as a testing method, and presented the theory to Kenneth Heilman, a professor of neurology at the University of Florida. So what’s the connection between smell and Alzheimer’s?

The ability to smell is associated with the first cranial nerve and is often the first one to be degraded in cognitive decline. Peanut butter is what you call a “pure odorant”, so it is only detected by the olfactory nerve and is very easy to access.

“Dr. Heilman said, ‘If you can come up with something quick and inexpensive, we can do it,’” Stamps says.

Basically, they asked patients to participate of this test, which only included a tablespoon and a ruler. The patient closed his or her eyes and mouth and blocked one nostril while the clinician opened the peanut butter container and placed it close to the open nostril. The clinician then moved the peanut butter 1 cm closer to the nostril and asked the patient if he/she felt the peanut butter smell, then repeated the entire procedure with the other nostril, after a 90 second period delay. People with early stages of Alzheimer’s had a dramatic difference between the left and right nostril performance – the left nostril was impaired, detecting the smell at an average of 10 cm closer.

In other types of dementia, the patients had almost no difference between the left and right nostril.

“At the moment, we can use this test to confirm diagnosis,” Stamps says. “But we plan to study patients with mild cognitive impairment to see if this test might be used to predict which patients are going to get Alzheimer’s disease.”

This test could be incredibly useful especially in less developed areas of the world, where clinics don’t have access to the equipment necessary to conduct traditional tests.

“We see people with all kinds of memory disorders,” Heilman says. Many tests to confirm a diagnosis of Alzheimer’s disease or other dementias can be time-consuming, costly, or invasive. “This can become an important part of the evaluation process.”