Tag Archives: Alzheimer

Playing video games improves spatial orientation, memory formation and strategic planning

Parents usually don’t encourage their kids to play computer games, even though by now, several studies have established significant benefits that come with the game. This most recent study from the Max Planck Institute showed that even playing a game as simple as Super Mario 64 results in increased size in brain regions responsible for spatial orientation, memory formation and strategic planning as well as fine motor skills.

super marios

The positive effects of video games could also be used to target psychiatric disorders, researchers explain.

To investigate just how video games affect the brain physically, scientists in Berlin asked 23 adults (mean age: 24) to play the video game “Super Mario 64” on a portable Nintendo XXL, for 30 minutes a day, over a period of two months. When compared to the control group, the gaming group showed increases of gray matter in the right hippocampus, right prefrontal cortex and the cerebellum, measured using MRI. Those areas are responsible for complex functions such as memory formation, strategic planning, spatial navigation, and fine skill hands.

“While previous studies have shown differences in brain structure of video gamers, the present study can demonstrate the direct causal link between video gaming and a volumetric brain increase. This proves that specific brain regions can be trained by means of video games”, says study leader Simone Kühn, senior scientist at the Center for Lifespan Psychology at the Max Planck Institute for Human Development.

videoame-effects-on-brain

The researchers are quite certain that their results can also be used for patients with mental disorders in which brain regions are altered or reduced in size – such as Alzheimer’s, PTSD or schizophrenia. Of course, playing computer games is far more acceptable than more intrusive procedores.

“Many patients will accept video games more readily than other medical interventions,” said Jürgen Gallinat, psychiatrist and co-author of the study at Charité University Medicine St. Hedwig-Krankenhaus.

Scientific Reference: S Kühn, T Gleich, R C Lorenz, U Lindenberger, J Gallinat, Playing Super Mario induces structural brain plasticity: gray matter changes resulting from training with a commercial video game, Molecular Psychiatry, 2013, DOI: 10.1038/mp.2013.120

EDIT: We’ve published an interview with Simone, which you can read HERE. Be sure to check it out, lots of valuable information there!

Pluripotent Stem Cells

Massive database of of 1,500 stem cell lines derived from diseased cells set to aid drug development

Pluripotent Stem Cells

The StemBANCC project, developed as a joint effort between the European Union and Europe’s pharmaceutical industry, is set to culture 1,500 pluripotent stem cell lines derived from the cells of diseased individuals like Alzheimer’s patients is currently planned. Using this massive database, researchers will be able to achieve much smoother and faster drug screening process in order to counter these diseases.

The 50 million euros project human-induced pluripotent stem cells as a drug discovery platform to treat the following 8 common diseases: Alzheimer’s disease, Parkinson’s disease, autism, schizophrenia, bipolar disorder, migraine, pain and diabetes.

Stem cells have been hailed as the basis for developing miracle drugs by the media on countless occasions. The project’s aims are not to derive drugs from stem cells, however, but to ease the development of mainstream drugs, that are a lot cheaper, by offering a drug screening platform. It’s one thing to test drugs on mice, and another thing to test them on human cells, more importantly on diseased cells.

For instance skin cells from a Parkinson’s patient can be turned into  pluripotent stem cells that can then be turned into neurons. This would offer researchers an amazing tool. Sure scientists can do this already, but when the project will be live, they could simply order the kind of stem cells they require for their research and be done with it.

Zameel Cader, neurologist at the University of Oxford and a leader on the project, told Nature, “We’re specifically trying to develop a panel of lines across a range of diseases that are important to address. There isn’t another institution that’s doing this at the same scale across the same range of diseases.”

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MRI scan brain white matter

Keeping the brain healthy with age: reading, writing or playing games

A new study found a direct correlation between the frequency of cognitive activity at later life and brain health. As we age, the brain’s structural integrity begins to dwindle, however these effects can be hampered to a certain degree by engaging in intellectual activities like reading, writing or playing chess. Any kind of activity that puts strain on the intellect later on in life will contribute to a healthier brain, the study found.

MRI scan brain white matter

(c) Vasireddi, A. et al./RSNA

Konstantinos Arfanakis, Ph.D., and colleagues from Rush University Medical Center and Illinois Institute of Technology in Chicago enlisted 152 elderly participants for their study, mean age 81 years, from the Rush Memory and Aging Project, a large-scale study looking at risk factors for Alzheimer’s disease. All the participants, however, were completely healthy and had no signs of dementia or mild cognitive impairment. The participants were asked to grade from 1 to 5 the frequency with which they participated in a list of mentally engaging activities during the last year.

The participants were then underwent brain MRI using a 1.5-T scanner within one year of clinical evaluation, time in which the scientists looked at a certain factor in particular –  diffusion anisotropy, a measure of how water molecules move through the brain. Generally, water molecules travel  easier in a direction parallel to the brain’s axon and harder  perpendicular to the axons, because it is impeded by structures such as axonal membranes and myelin. By using data gathered from the magnetic resonance imaging (MRI), the researchers were able to map how diffusion anisotropy behaved in each participant.

“This difference in the diffusion rates along different directions increases diffusion anisotropy values,” Dr. Arfanakis said. “Diffusion anisotropy is higher when more diffusion is happening in one direction compared to others.” The anisotropy values in white matter drop, however, with aging, injury and disease.

“In healthy white matter tissue, water can’t move as much in directions perpendicular to the nerve fibers,” Dr. Arfanakis said. “But if, for example, you have lower neuronal density or less myelin, then the water has more freedom to move perpendicular to the fibers, so you would have reduced diffusion anisotropy. Lower diffusion anisotropy values are consistent with aging.”

Thus, a significant associations between the frequency of cognitive activity in later life and higher diffusion anisotropy values in the brain was found. If you think you’re still too young to take note of this kind of information, consider that diffusion anisotropy drops gradually beginning at around age 30. Moreover, it’s good practice to keep engaged in intellectual activities all your life, not only from brain health related reasons alone. Most often, the rewards that come from intellectual stimulation pass their physical sense.

“Several areas throughout the brain, including regions quite important to cognition, showed higher microstructural integrity with more frequent cognitive activity in late life,” said Dr. Arfanakis. “Keeping the brain occupied late in life has positive outcomes.”

“In these participants, we’ve shown an association between late-life cognitive activity and structural integrity, but we haven’t shown that one causes the other,” Dr. Arfanakis said. “We want to follow the same patients over time to demonstrate a causal link.”

Findings were presented at the Radiological Society of North America 2012 Scientific Assembly and Annual Meeting.

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alzheirmer's disease

Earliest signs of Alzheimer’s found in 20-something year olds. Provides hints for prevention treatments

Alzheimer’s is a devastating disease for both patients and their families that typically affects the elderly in large proportions. Detecting the disease in its early phase gives the best chances for effective treatment. A team of scientists recently performed an extensive survey in a group of  20-somethings, marking the earliest ever detection of early-onset dementia warning signs and paving the way for new treatments.

alzheirmer's diseaseThe scientists studied people aged 18 to 26 who carried a gene mutation that made them more vulnerable to early-onset and familial Alzheimer’s disease. When compared to non-carriers, they found distinct differences like certain proteins in blood and cerebrospinal fluid and brain changes. These are early signs that hint towards Alzheirmer’s even 25 years before the disease even gets the chance to show its symptoms.

“Early-onset and familial Alzheimer’s disease is relatively uncommon but terribly distressing for the individuals and their family,” said Associate Professor Michael Valenzuela, Leader of Regenerative Neuroscience Group, at the University of Sydney’s Brain & Mind Research Institute, who was not involved in the study.

“If we are to intervene to help stop or slow the disease, when? Clearly, 20 years before symptoms there are already major brain changes; does that mean we need to intervene even earlier (adolescence or childhood)? How realistic is this, particularly if such an intervention were to have significant risks?”

The findings are indeed monumental for those suffering from early onset or familial Alzheimer, but follow-up studies are required to see whether these apply to people with late-onset Alzheimer’s disease that do not carry the genetic mutation present in this study’s group of subjects. “Then a simple blood test may be possible in the future which can indicate people at risk.”

Findings were published in The Lancet Neurology.

Intracellular controlled release of molecules within senescent cells was achieved using mesoporous silica nanoparticles (MSNs) capped with a galacto-oligosaccharide (GOS) to contain the cargo molecules (magenta spheres; see scheme). The GOS is a substrate of the senescent biomarker, senescence-associated β-galactosidase (SA-β-gal), and releases the cargo upon entry into SA-β-gal expressing cells.

Intelligent nanoparticles drop anti-aging cargo

A group of researchers have successfully tested a novel nanodevice treatment, in which intelligent nanoparticles selectively open and release drugs which target aging cells. The approach could render results when treating patients suffering from diseases involving tissue or cellular degeneration such as cancer, Alzheimer’s, Parkinson’s, accelerated aging disorders (progeria). It could also boosts results in the cosmetic industry, where anti-aging products are always welcomed.

Intracellular controlled release of molecules within senescent cells was achieved using mesoporous silica nanoparticles (MSNs) capped with a galacto-oligosaccharide (GOS) to contain the cargo molecules (magenta spheres; see scheme). The GOS is a substrate of the senescent biomarker, senescence-associated β-galactosidase (SA-β-gal), and releases the cargo upon entry into SA-β-gal expressing cells.

Intracellular controlled release of molecules within senescent cells was achieved using mesoporous silica nanoparticles (MSNs) capped with a galacto-oligosaccharide (GOS) to contain the cargo molecules (magenta spheres; see scheme). The GOS is a substrate of the senescent biomarker, senescence-associated β-galactosidase (SA-β-gal), and releases the cargo upon entry into SA-β-gal expressing cells.

Senescence is a physiological process of the body to eliminate aged cells or ones with alterations that may compromise their viability. In young, healthy bodies the senescence mechanisms prevents the accumulation of aged cells (senescent) in organs and tissues, which disrupts their proper functions, and sometimes lead to the apparition of tumors. As we continue to age, though, senescent accumulation is inevitable and age related diseases surface. The elimination of these cells would slow down the appearance of diseases associated with aging.

“The nanodevice that we have developed consists of mesoporous nanoparticles with a galactooligosaccharide outer surface that prevents the release of the load and that only selectively opens in degenerative phase cells or senescent cells. The proof of concept demonstrates for the first time that selected chemicals can be released in these cells and not in others,” says Ramón Martínez Máñez, researcher at the IDN Centre — Universitat Politècnica de València and CIBER-BBN member.

The scientists tested the new nanodevice in cell cultures derived of patients with accelerated aging syndrome dyskeratosis congenita. These cell cultures are characterized by a high concentration of senescent cells, due to high levels of beta-galactosidase activity – an enzyme which is associated with senescence. The researchers designed nanoparticles that open when the enzyme is detected release their contents in order to eliminate senescent cells, prevent deterioration or even reactivate for their rejuvenation.

“There are a number of diseases associated with premature aging of tissues, many of which affect very young patients and for whom there is no therapeutic alternative, as in the case of DC or aplastic anemia. Other diseases affect adults, as idiopathic pulmonary fibrosis or liver cirrhosis. These nanoparticles represent a unique opportunity to selectively deliver therapeutic compounds to affected tissues and rescue their viability and functionality” explains Rosario Perona, researcher at the Instituto de Investigaciones Biomédicas (CSIC/UAM) and CIBERER member.

The next step of this research is to test the devise with therapeutic agents and validate it in animal models.

“As far as we know this is the first time that a nanotherapy for senescent cells has been described. Although there is still far to go from these results to the possible elimination of senescent cells or rejuvenation therapies, we believe that our research may open new paths for developing therapies for the treatment of age-related diseases,” says Ramón Martínez Máñez.

Findings were published in the journal Angewandte Chemie International.

Protein re-assembly

New method allows visualizing of protein self-assembly – paves way for nanotech against diseases

Be it a bacteria or a fully complex being, say a human, all living, biological organisms undergo lighting fast protein structure reassembly in response to environmnetal stimuli. For instance,  receptor proteins in the sinus are stimulated by various odor molecules, basically telling the organism that there’s food nearby or it’s in the vicinity of danger (sulphur, methane, noxious fumes). By studying these mechanisms, scientists can better understand these process. A great leap further in the field was achieved by researchers at  the University of Montreal, who’ve managed to image how proteins self-assemble.

Protein re-assembly

Here shown are two different assembly stages (purple and red) of the protein ubiquitin and the fluorescent probe used to visualize these stage (tryptophan: see yellow). Credit: Peter Allen.

Understanding and mapping these process helps pave a broader, more plastic picture of how organisms function from a molecular assembly mechanism point of view, but maybe most importantly aids in pinpointing assembly errors. Both Alzheimer’s and Parkinson’s, two of the most devastating neural degenerative disease currently plaguing mankind, are caused by errors in molecular assembly. According to Professor Stephen Michnick, the research is expected to help bioengineers design new molecular machines for nanotechnology applications which might fight these diseases.

“In order to survive, all creatures, from bacteria to humans, monitor and transform their environments using small protein nanomachines made of thousands of atoms,” explained Michnick.

Proteins are composed of linear structural chains of amino acids, which have the capability to self assemble at the rate of thousandth of a second into a nanomachine by virtue of millions of years of evolution. Determining how these proteins self-assemble is a crucial goal in biotechnology at the moment, however, this extremely fast assembly velocity, as well as the numerous possible combinations, makes it extremely difficult.

“One of the main challenges for biochemists is to understand how these linear chains assemble into their correct structure given an astronomically large number of other possible forms,” Michnick said.

Researcher Dr. Alexis Vallée-Bélisle expressed similar sentiments.

“To understand how a protein goes from a linear chain to a unique assembled structure, we need to capture snapshots of its shape at each stage of assembly,” Vallée-Bélisle noted.

The researchers sought to overcome these setbacks, and successfully established a new method for visualizing the process of protein assembly by attaching fluorescent probes at all points on the linear protein chain.

“The problem is that each step exists for a fleetingly short time and no available technique enables us to obtain precise structural information on these states within such a small time frame. We developed a strategy to monitor protein assembly by integrating fluorescent probes throughout the linear protein chain so that we could detect the structure of each stage of protein assembly, step by step to its final structure.”

However, Vallée-Bélisle emphasized that the protein assembly process “is not the end of its journey,” as a protein can change, via chemical modifications or with age, to take on different forms and functions.

“Understanding how a protein goes from being one thing to becoming another is the first step towards understanding and designing protein nanomachines for biotechnologies such as medical and environmental diagnostic sensors, drug synthesis of delivery,” he added.

The research is funded by Le fond de recherché du Québec, Nature et Technologie and the Natural Sciences and Engineering Research Council of Canada. The findings were published in the journal Nature Structural & Molecular Biology.’

source: U Montreal.

Healthy Brain vs Alzheimer's Disease

Drug used for skin cancer might provide remarkable results for Alzheimer’s patients

Researchers report that after testing on lab mice an FDA-approved drug, used as treatment for skin cancer, that significant improvements in cognitive recovery were signaled, shinning a new ray of hope for Alzheimer patients.

Neuroscientists Case Western Reserve University School of Medicine discovered that bexarotene, a skin cancer drug, remarkably 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, which is closely related to Alzheimer’s progression, and thus work wonders! Mice inflicted with Alzheimer’s were given the drug, and all showed clear signs of cognitive recovery. Moreover the speed of recovery was astonishing!

Healthy Brain vs Alzheimer's Disease In a healthy brain, amyloid proteins are naturally broken down and eliminated. Patients suffering from Alzheimer’s, however, lose this ability, allowing for amyloid plaques to form, which have a significant contribution towards brain cell degradation, ultimately leading to dementia.

“This is a particularly exciting and rewarding study because of the new science we have discovered and the potential promise of a therapy for Alzheimer’s disease,” study author, professor Gary Landreth told the Press Association.

The scientists involved in the study, however, stress that their research is still in its infancy, considering the discovery that bexarotene might work for Alzheimer’s suffers as well was made fairly recently. Success in mice does not guarantee it will work for humans as well – it wouldn’t be the first time.

“Our next objective is to ascertain if it acts similarly in humans,” professor Landreth added.

Clinical trials will be necessary before scientists may assert whether bexarotene could prove beneficial for people with Alzheimer’s, as well as assess any potential side-effects.

The study was published in the journal Science.

[image source]

Memory deficits of the elderly may be reversed

A team of researchers from Yale University have shown at a cellular basis why we tend to be more forgetful as we age, and claim that the condition may be reversed.

There’s no secret to the fact that an elderly person has a much weaker memory than the one he did at 20 years of age, but the whole process which leads to this degradation is still far from being entirely known. The researchers behind the study, recently published in the journal Nature, believe neural networks in the brains of the middle-aged and elderly have weaker connections and fire less robustly than in youthful ones.

“Age-related cognitive deficits can have a serious impact on our lives in the Information Age, as people often need higher cognitive functions to meet even basic needs, such as paying bills or accessing medical care,” says Amy Arnsten, professor of neurobiology and psychology at Yale University. “These abilities are critical for maintaining demanding careers and being able to live independently as we grow older.”

Experimenting, they looked for age-related changes in the activity of neurons in the prefrontal cortex (PFC), the area of the brain that is responsible for higher cognitive and executive functions, of variously aged animals. The PFC network of neurons is one of the brain’s most active regions when a person isn’t asleep, firing up signals constantly – this is where all the “working memory” magic is.

A neat working memory is essential for complex tasks such as reasoning, comprehension and learning. It also controls short-memory, allowing you to remember simple things like where your parked the car or put your keys, while being constantly updated and refreshed.

Arnsten and colleagues analyzed the PFC signals in young, medium-aged and old animals. They observed that young animals could maintain a higher rate of signal shooting in the working memory than those much older. Scientists looking for a reason for this, believe the PFC of older animals accumulate excessive levels of a signaling molecule called cAMP, which can open ion channels and weaken prefrontal neuronal firing.

By using agents that inhibit the generation of cAMP in the brain, they were able to to restore more youthful firing patterns in the aged neurons, albeit not exactly like those found in a young specimen – the improvements were dramatic, however. One of such agents employed was guanfacine, a neural enhancer already prescribed to children with PFC deficiencies and for hypertension treatment.

A clinical trial will shortly commence headed by Yale School of Medicine to see what kind of improvements guanfacine might have for the working memory in human subjects. Scientists doubt however that the substance might be used for treatments against Alzheimer or other forms of dementia.

An unhealthy lifestyle leads to brain shrinkage later on, study says

The latin phrase “mens sana in corpore sano” has been put to the test by researchers who wanted to study what kind of repercussions an unhealthy lifestyle has on the mind. What they found was a dramatic increase in brain damage and dementia cases among subjects who have experienced high blood pressure, diabetes, smoking and obesity in middle age.

The study, published in today’s edition of the journal Neurology, worked around the already available famous Framingham Heart Study, which has followed residents of Framingham, Mass., and now their offspring, for more than 60 years. Using data from this extensive research, scientists only chose a small subset of 1,400 people to study their habits and general health status and see how they correlate to the various potential brain afflictions one might posses later on in life.

Using brainteaser tests and routine MRI scans, the researchers’ results were staggering – each potential hazard like hypertension, diabetes, smoking and obesity was linked to a different cognitive impairment.  As such, people with high blood pressure had a much greater risk of succumbing to vascular damage in their brains, than those with normal blood pressure. Diabetics lost brain volume in the hippocampus, which, among other functions, converts short-term memory into long-term memory – a great risk factor for Alzheimer. The worst off were smokers  – they were found to experience a brain volume shrinkage in overall and in the hippocampus at a faster rate than nonsmokers, while at the same time, coupled with hypertension, they also showed white matter vascular damage.

Obesity was found to be extremely troublesome to the mind’s health as well. Obese people were more likely to score lower at test scores for various brain tasks, such as memory and abstract thinking, than people with a normal body mass index. Actually, scientists found that the more obese a person was, the greater the brain shrinkage and the greater the risk of dementia. In a study we reported on a few months ago, another group of researchers reached the same result when they published a paper in which they showed how obesity is linked to dementia.

Glowing dog

Scientists genetically engineer glowing dog

In what’s maybe the most startling research I’ve been granted to read about recently, scientists from South Korea at Seoul National University, home to the world’s only strictly genetic engineering curricula, have successfully created a dog that can glow in the dark.

The genetically modified female beagle, named Tegon, was born in 2009 using a cloning technique which could help find cures for human diseases such as Alzheimer’s and Parkinson’s. Far from being a twisted joke, the whole experience can be marked as practice. By inserting genes into dogs that cause human illnesses and then swithiching these on and off, researchers are able to study them and come up with cures.

Glowing dog

(c) Genesis

The dog’s remarkable translucent ability was rendered possible after the South Korean scientists added eGFP (enhanced green flourescent protein) to the nucleus of a cell and placing it inside of an egg. The researchers, who completed a two-year test, said the ability to glow can be turned on or off by adding a drug to the dog’s food, called doxycycline.

“The creation of Tegon opens new horizons since the gene injected to make the dog glow can be substituted with genes that trigger fatal human diseases,” lead researcher Lee Byeong-chun said.

The same somatic cell nuclear transfer technology, which was used to create Tegon, was employed for the creation of Snoopy, the first cloned dog, in 2005 at the same university. Two years ago, the same scientists, produced Ruby Puppy, or Ruppy, a red-fluorescent-glowing dog.

The whole $3 million study can be read in detail at Genesis, the Journal of Genetics and Development.

reuters

Over half of Alzheimer’s cases could be avoided

According to a study conducted by Deborah Barnes, PhD, a mental health researcher at the San Francisco VA Medical Center, more than half of all Alzheimer’s cases could be prevented through lifestyle changes or light treatment.

Analyzing thousands of cases worldwide, she concluded that the biggest impacting factors on Alzheimer that can be modified are, in descending order, low education, smoking, physical inactivity, depression, mid-life hypertension, diabetes and mid-life obesity. In the United States for example the biggest modifiable factors are physical inactivity, depression, smoking, mid-life hypertension, mid-life obesity, low education and diabetes. Together, these factors are associated with 51 percent of Alzheimer’s cases worldwide (17.2 million cases) and up to 54 percent of Alzheimer’s cases in the United States (2.9 million cases), according to Barnes.

“What’s exciting is that this suggests that some very simple lifestyle changes, such as increasing physical activity and quitting smoking, could have a tremendous impact on preventing Alzheimer’s and other dementias in the United States and worldwide,” said Barnes, who is also an associate professor of psychiatry at the University of California, San Francisco.

However, it has to be said that the conclusions are drawn based on the idea that there is a causal association between each risk factor and Alzheimer’s disease.

“We are assuming that when you change the risk factor, then you change the risk,” Barnes said. “What we need to do now is figure out whether that assumption is correct.”

Remember and forget at the flick of a button

A team of neuro-scientists have managed to restore lost memories to rats by activating a part of their brains through an artificial memory chip – just like a sort of neuro-prosthesis. Further advances backed by this study might lead to the development of important leaps in long-term memory treatment, providing relief for Alzheimer or dementia patients.

Researchers from Wake Forest University and the University of Southern California, trained rats to perform certain tasks like having to pull a lever to receive water. In one case, scientists distracted the rats, forcing them to remember which lever they had to pull. During all of this, researchers attached a set of electrodes to the rat’s brain, connected to two areas in the hippocampus, called CA1 and CA3. The hippocampus is responsible for bridging short-term memory with long-term. As such, as the rats performed various tasks their brain signal between the two regions was monitored.

The rats were then drugged, thus interrupting communication between CA1 and CA3. Immediately, they didn’t know what lever to press next, and which succession respectively, as their long-term memory was basically fried.

“The rats still showed that they knew ‘when you press left first, then press right next time, and vice-versa,’” Theodore Berger said, a biomedical engineering professor at USC and lead author of the study. “And they still knew in general to press levers for water, but they could only remember whether they had pressed left or right for 5-10 seconds.”

The team then attached an artificial hippocampus, which duplicated the natural signals between CA1 and CA3. When turned on, the previously recorded action and order of manipulating the levers stored in CA1 was successfully communicated back to CA3, allowing the rats to perform normally again. When switched off, the rats reverted back to not remembering which action to perform next.

“Flip the switch on, and the rats remember. Flip it off, and the rats forget,” Berger said.

The research, published in the Journal of Neural Engineering, looks terribly exiting, although applications in humans are a long way from being developed. It proves however that neural signals and patterns which are recorded and stored, can be activated though a neural impulse. A device attached to the brain of a patient suffering from dementia, for example, might help him enhance his short-term memory beyond that of a gold fish and thus make him more independent, make his life livable. Researchers plan to text the device next on monkeys, which usually is the last step before human experimentation.

Also, who remembers this episode?

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Obesity linked to dementia

Obesity linked to dementia, study says

Obesity linked to dementiaAccording to a recently published study reported by Swedish scientists, people who are obese and middle aged are up to four times more likely do develop dementia than people of normal weight.

Published in the journal Neurology, the research was conducted 8,534 Swedish twins over the age of 65, of which data showed that 350 had been diagnosed with Alzheimer or vascular dementia, while a further 114 had possible dementia. Using records of the patient’s past weight compared to their age, researchers found that middle aged people who were overweight are 71 per cent more likely to develop dementia than for people who are of a normal weight.

An person is considered overweight when his body mass index (BMI) falls between the 25 and 30 ratio, while a ratio between 20 and 25 corresponds to a person of normal weight. What’s extremely curious, and more or less supports the hypothesis of the link between dementia and obesity, is that persons falling under a BMI greater than 30 (clinically obese) in their midlife had an almost four times (300%) higher risk of dementia.

“Currently, 1.6 billion adults are overweight or obese worldwide and over 50% of adults in the US and Europe fit into this category,” said Weili Xu of the Karolinska Institutet in Stockholm, who led the research. “Our results contribute to the growing evidence that controlling body weight or losing weight in middle age could reduce your risk of dementia.”

lmost 30% of those in the study, 2,541 in total, had been either overweight or obese between 40 and 60 years of age.

“Although the effect of midlife overweight on dementia is not as substantial as that of obesity, its impact on public health and clinical practice is significant due to the high prevalence of overweight adults worldwide,” said Xu.

Scientists still don’t know why exactly overweight is linked to obesity, by they believe higher body fat is associated with diabetes and vascular diseases, which are related to dementia risk.

Susanne Sorensen, head of research at the Alzheimer’s Society, said: “This robust study adds to the large body of evidence suggesting that if you pile on the pounds in middle age, your chances of developing dementia are also increased.By eating healthily and exercising regularly, you can lessen your risk of developing dementia. Not smoking and getting your cholesterol and blood pressure checked regularly is also very important.”

Sorensen said that further research was needed to find the links between being overweight and dementia. “One in three people over 65 will die with dementia, yet research into the condition is desperately underfunded.”

It is believed that about one in 20 people over the age of the 65 has some form of dementia.  Similar studies have been made in 2004 and 2005, both leading to the same conclusion that indeed obesity can influence the development of dementia.

Take your brain to a whole new level – learn as a child does

The brains of adults can grow significantly in a staggeringly short amount of time if you just start learning like children do, according to research that had the purpose of treating braind disorders; they seem to have stumbled into something different, but extremely interesting.

The researchers unexpectedly discovered that adult brains can grow in only two hours (!) just by imitating the rapid learning that takes place during childhood. Scientists have long known that the brains of children increase rapidly, but there has been a growing interest in finding out more about this phenomena – and for good reason, because the potential here is huge. Other recent studies have shown that the brain is still plastic and the grey matter can grow after experiences that last even only a few weeks.

“Our finding suggests that the adult human brain is far more plastic than previously believed,” researcher Li-Hai Tan, a cognitive neuroscientist at the University of Hong Kong, stated. “We are very excited about the finding, because we think that it offers hope to adult people with brain development disorders — with appropriate intervention strategies, adults’ brains may still be able to quickly develop structure to acquire skills. This will be a welcome relief to many families.”

The scientists were actually analyzing the effects that language has on color perception, a hot matter of debate; more than half a century ago, linguist Benjamin Lee Whorf made a startling theory, suggesting that language can affect how one thinks and perceives the world. Tan and his colleagues wanted to check if these effects can be seen at cellular levels.

The volunteers were asked to learn made-up words for two shades of green and two shades of blue and the task was to mimic the rapid and intense learning done during childhood. They were asked to name these colours when flashed on a screen, as well as identify if the colours and the words next to them matched.

After only five training sessions done in three days, and a total training time of only 1 hour and 48 minutes, brain scanst revealed that there had been a rapid increase in gray matter in the left visual cortex of the volunteers, especially in the areas of the brain linked with colour vision and perception.

“We were so surprised, we could not believe it — the adult human brain structure changes so fast,” Tan said.

The results are absolutely spectacular, but the permanence of these changes is still a matter of debate.

“It remains to be seen if those motor tasks might lead to a quick change of the brain at the macroscopic level — that is, gray matter,” Tan said.

Nonetheless, it’s an absolutely stunning study in my opinion, and I truly hope further reseach will be continued as soon as possible.

Gene therapy for Parkinson disease boasts remarkable results

While gene-therapy is still regarded as a very innovative practice, it seems like the procedure might take traction as of today when remarkable results were concluded after the first successful double-blind gene therapy for Parkinson disease. In the case of this dreadful disease, medical researchers injected patients with a a gene that codes for glutamic acid decarboxylase (GAD), an enzyme that catalyses production of an inhibitory neurotransmitter called gamma-aminobutyric acid (GABA).

Usually Parkinson patients produce too little GABA in their brains, and as a result overstimulation in an area of the brain called the subthalamic nucleus occurs, which in turn inhibits dopamine secretion, which is vital for movement. This is why Parkinson patients are described as having tremors, sluggish movements, rigid muscles and impaired posture and balance.

Andrew Feigin of the Feinstein Institute for Medical Research in Manhasset, New York, and colleagues conducted a double-blind test for GAD gene-therapy on a group of 65 patients. In this particular case, double-blind test refers to the fact that patients were grouped into patients who received a placebo surgery (a simple saline solution injected in the back of the skull) and those receiving real surgery (the skull was drilled and a virus containing the GAD gene was injected). Neither patients, nor researchers knew who was given a placebo or not when test results came in, apart from the surgeons – hence the double-blind test.

In the trial, 22 Parkinson’s patients had a gene inserted in their brains to produce more GABA, while twenty-three patients received the placebo. Six months later, researchers analyzed the results and came up with something remarkable – gene therapy patients showed improvements in their motor functions of 23.1 per cent, while also remarkably interesting those who were given a sham procedure scored an improved of  just 12.7 per cent.  The researchers rated the patients’ symptoms, including the severity of tremors and stiffness, and came up with a single “motor score” that represented how well they could move.

The treatment is intended for a subgroup of Parkinson’s patients — those who do not respond to medication very well. Of the 1 million to 1.5 million Americans with Parkinson’s, about 10 to 15 percent of them, or 100,000 to 200,000 people, fit into this category, said study researcher Dr. Michael Kaplitt, vice chairman for research in the Department of Neurological Surgery at Weill Cornell Medical College in New York.

The therapy came just in time for Dr. Walter Liskiewicz, 60, a Jackson oral surgeon so disabled with Parkinson’s that he could not walk before his July 2009 procedure.Now, he not only walks with a cane but he’s back playing a harmonica and writing smooth jazz.

The study “brings us much closer to having a gene therapy that might be ready for general use,” Kaplitt said. The work paves the way for gene therapies for other types of brain diseases, he said. “I think we are now helping to facilitate and to accelerate the development of a whole host of gene therapies … for diseases such as Alzheimer‘s disease, epilepsy [and] depression,” he said.

The results are indeed very satisfying, but since the actual procedure was made only on 22 Parkinson patients, further investigation is required.

image via knowabouthealth.com

Increasing brain enzyme may slow Alzheimer’s

The fight against Alzheimer’s is a harsh and rugged one, and despite numerous advancements, there still isn’t a definitive cure for the disease around – or a fail proof way to detect it in the early stages.. Still, if you can’t defeat it, it’s still better to slow it down a little, and that’s exactly what researchers from Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center (LA BioMed) had in mind. They found that increasing the most abundant brain peptidase in mammals significantly slows down the accumulation of tau proteins that are toxic to nerve cells and can cause or amplify Alzheimer’s, as well as other forms of dementia.

The study, published in Human Molecular Genetics showed that the increase of these peptidase have no negative side effects, but does remove tau proteins in the neurons.

“Our research demonstrated that increasing the brain enzyme known as PSA/NPEPPS can effectively block the accumulation of tau protein that is toxic to nerve cells and slow down the progression of neural degeneration without unwanted side effects,” said Stanislav L. Karsten, PhD, the corresponding author for the study and a principal investigator at Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center (LA BioMed).

“These findings suggest that increasing this naturally occurring brain peptidase, PSA/NPEPPS, may be a feasible therapeutic approach to eliminate the accumulation of unwanted toxic proteins, such as tau, that cause the neural degeneration associated with the devastating effects of Alzheimer’s disease and other forms of dementia.”

Alzheimer’s disease affects 2-4 million people in America only, but it is believed that this number will increase dramatically as popullation continues to age.

New ways to detect Alzheimer found

Alzheimer is one of the nastiest diseases you can get; it is a degenerative disease that affects your brain cells, and as far as we know, the best way to prevent it is by being mentally active throughout your life. The most recent study conducted about it takes a look at ways of detecting the disease in its initial stages. The results give scientists a greater understanding of the changes that are triggered during the initial stages, and may help individuals at risk.

According to the Alzheimer Association, 5.3 million people are suffering from the disease, and as world population continues to age, it will definitely affect more and more people, so detecting Alzheimer early, in potentially treatable stages could be the key to fighting it.

“Identifying those at risk for Alzheimer’s and developing new treatments for nervous system disorders is a social imperative,” said press conference moderator Sam Sisodia, PhD, of the University of Chicago, an expert on the cellular biology of proteins implicated in Alzheimer’s disease. “These studies are evidence that we’re making real progress to overcome this tragic epidemic.”

Also, the research also found that a new vaccine tested in mice could protect against memory loss caused by Alzheimer disease, without any potential harmful side effects. However, with this study, as well as the other ones before it, the progress is not that big. There still isn’t a single definite way of detecting or treating the disease, but hopefully, these small steps forward will pave the way for it as time passes.

Source

Function found for Alzheimer protein

Recently, numerous developments in Alzheimer research have been made, including a ‘brain pacemaker‘ and the discovery of an extremely promising chemical, p7c3, that might help treat patients. This time, researchers went for a different approach; what happens in Alzheimer is that the brain basically grows some lumps of protein, developing formations known as amyloid plaques that prevent it from working properly. This study, revealed in the September 17th print issue of Cell seems to have found a way to make something useful with the amyloid precursor protein (APP for short), the main ingredient in these plaques.

At its very core, APP is a iron oxidase whose job is to transform iron into a safer form and ready it for transport throughout the body. If it doesn’t work right, like in Alzheimer’s disease, iron levels get really high and they become toxic.

“This opens a big window on Alzheimer’s disease and iron metabolism,” said Ashley Bush of The Mental Health Research Institute, University of Melbourne.

“Although people have attributed several important physiological roles to APP,” added Jack Rogers of Harvard Medical School, “this now gives us an idea of what this critical protein does to underpin its role in iron metabolism.”

However, this amyloid alone can not explain what happens in the brain during Alzheimer. In order to do that, you have to look deeper and analyze the different metal concentrations in the brain.

“There has been a lot of attention on amyloid, but it seems it is not a simple matter of amyloid as the sole culprit,” Bush said. For one thing, trials of drugs designed to target and clear amyloid plaques haven’t worked as intended.

The findings suggest that zinc may be the ideal target in the war on Alzheimer.

“Our findings authenticate zinc as a target,” Bush said. “It really makes it look like an attractive place to hit.”

Although researchers don’t want to raise hopes too much, an Alzheimer cure, or at least a way to significantly slow down the progression of the disease seems more and more close.

Alzheirmer

Improved memory in Alzheimer patients with the help of a ‘brain pacemaker’

AlzheirmerAlzheimer’s  is one of the most common, yet devastating, form of dementia which currently accounts for more than 5 million patients in the US alone, most of which are elderly. By now, I’m sure most of you know how this terrible disease manifests itself, enough to make a sexagenarian forget his children and nephews. What’s tragic is that Alzheimer is irreversible and, at present date despite countless efforts and billions of dollars worth of investments, can not be cured.

Research however is doing its fair part and not a day passes without some kind of visible progresses being made. The latest initiative comes from Canada where a group of researchers have managed to insert a deep brain stimulator (DBS), a small device comparable to a pacemaker, which allegedly drastically improves the memory of the subjects its been so far tested on. The research was conducted upon six subjects, out of which half showed signs of improvement during the course of a 6 to 12 month period.

“We showed that not only is this a safe procedure, but that the evidence is there to warrant a bigger trial,” according to Dr. Andres Lozano and colleagues at Toronto Western Hospital, who conducted the research. “Any amount of time that extends quality of life and quality years to someone with Alzheimer’s may be a benefit.”

Lozano first discovered the potential for the brain pacemaker therapy, called Deep Brain Stimulation, to treat Alzheimer’s disease while treating a patient for obesity using DBS in 2003. He found that signaling areas of the brain triggered memories in the patient.

The theory behind this experiment lies in the principle  that electrical stimulation of structures deep in the brain, including the hypothalamus, might be able to improve Alzheimer symptoms. As such the six volunteers were each inserted with the “brain pacemaker”, after which they were supervised whole year. During this time numerous cognitive tests were subjected to time . Also, PET scans, a type of brain scan that measures metabolic activity, were used to assess the way the DBS device changed glucose metabolism in the brain, since Alzheimer is known to alter the glucose levels in the organism.

“Evaluation of the Alzheimer’s Disease Assessment Scale cognitive subscale and the Mini Mental State Examination suggested possible improvements and/or slowing in the rate of cognitive decline at 6 and 12 months in some patients,” according to the researchers.

The PET scans also show an improvement in the glucose metabolism, which usually are at abnormal levels among Alzheimer patients.

The study itself is still very restraint and Lozano suggests research at a larger scale is warranted considering the high potential DBS could have in helping patients improve memory or at least slow down the devastating Alzheimer.

“There is an urgent need for novel therapeutic approaches for Alzheimer’s disease. Modulating pathological brain activity in this illness with DBS merits further investigation.”

P7C3: a chemical to make brain cells grow (possible cure for Alzheimer)

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(c) Andrew Pieper, M.D., Ph.D., UT Southwestern Medical Center

A group of scientists from the University of Texas Southwestern Medical Center discovered a new chemical compound that helps newborn neurons grow into mature brain cells called P7C3. This particular chemical makes new neurons grow in the part of the brain that is integral to learning and memory! This means the research, funded in part by the National Institutes of Health, might lead to a treatment for Alzheimer’s disease thanks to P7C3’s neuroprotective mechanism.

The discovery was made after researchers infused lab mice with 1,000 different chemicals into their brains, systematically. “It was blind luck,” bluntly admit the researchers from the University of Texas Southwestern (UTS).

“This neuroprotective compound, called P7C3, holds special promise because of its medication-friendly properties,” explained Steven McKnight, Ph.D., who co-led the research with Andrew Pieper, M.D., Ph.D., both of University of Texas Southwestern Medical Center, Dallas. “It can be taken orally, crosses the blood-brain barrier with long-lasting effects, and is safely tolerated by mice during many stages of development.”

Various tests were made to see whether P7C3 can actually help stimulate the growth of new neurons, as well as the preservation of old neurons (this could in turn help aging people cope with dying brain cells). Researchers tested the chemical on mice carrying a genetic mutation that renders them almost completely incapable of producing new neurons in the dentate gyrus region – a perfect candidate. What happened next? Well, not only did new neurons form, but electrophysiological recordings also showed that processing in the dentate gyrus had been restored. “Sure enough, we had evidence that you can actually create new neurons that work,” McKnight said.

“This striking demonstration of a treatment that stems age-related cognitive decline in living animals points the way to potential development of the first cures that will address the core illness process in Alzheimer’s disease,” said NIMH Director Thomas Insel, M.D.

P7C3 is indeed a truly remarkable discovery, but scientists still know very little about how P7C3 works exactly, but further years of research and tests will follow, and a miracle drug might finally be developed. [via physorg.com]