Posts tagged alzheimer's disease
Articles and news from the latest research reports.
Greek scientists design early diagnosis tool for Alzheimer’s
An early diagnosis protocol for Alzheimer’s has been designed by researchers at the Ionian University in Greece, opening the way for the prevention and more effective treatment of the neurodegenerative disorder, which shows rapid deterioration and constitutes growing concern for modern societies.
The tool for the early diagnosis and prevention of Alzheimer’s disease dysfunctions is unique and has already attracted the strong interest of domestic and foreign pharmaceutical companies.
The research scientists have found the indices and their correlations that lead to an early diagnosis of the disease, through a hybrid diagnostic protocol based on the assessment of individual data.
A year ago the scientific research team discovered the “electric thrombosis” phenomenon, a mechanism that explains a series of dysfunctions, in the inner membrane of mitochondria affecting their number and operation, largely related with Alzheimer’s.
The team continued the research further by studying the mitochondrial membrane superconductor properties and other measurable biological factors before coming up with the early diagnosis tool for the disease.
What links Alzheimer’s disease, the bridges of Königsberg and Twitter?
A mathematical puzzle originating in 18th century Prussia has led to insights in fields as diverse as banking, social networking, epidemiology – and now Alzheimer’s disease
The progression of Alzheimer’s is accompanied by a buildup in the brain of amyloid plaque and the breakdown of communication between nerve cells. Recent research suggests that graph theory can provide fascinating insights into the faulty wiring behind the progressive memory loss of Alzheimer’s. But what exactly is graph theory?
To discover the origins of the theory we have to go back to the 18th century and the ancient Prussian city of Königsberg, now Kaliningrad – that tiny city state wedged between Poland and Lithuania. It was here that Leonard Euler solved the long-standing Bridges of Königsberg Problem, which has had a profound effect on the development of network theory.
Shortened telomere length tied to dementia, mortality risk
July 25, 2012
(HealthDay) — Shortened telomere length (TL) is associated with risks for dementia and mortality in a population of older adults, according to a study published online July 23 in the Archives of Neurology.
Lawrence S. Honig, M.D., Ph.D., from the Columbia University College of Physicians and Surgeons in New York City, and colleagues used real-time polymerase chain reaction analysis to determine TL in stored leukocyte DNA from 1,983 participants in a community-based study of aging. Participants were 65 years or older and blood was drawn at a mean age of 78.3 years. Participants were followed for a median of 9.3 years for mortality, and 9.6 percent developed incident dementia.
The researchers found that TL correlated inversely with age and was shorter in men than women. TL was significantly shorter in persons dying during follow-up compared with survivors, even after adjusting for age, sex, education, and apolipoprotein E genotype. TL was significantly shorter in the participants with incident and prevalent dementia, compared with those who remained dementia-free. Shorter TL correlated with earlier onset of dementia but this association was significant in women only.
"Our results show an association between shortened TL and mortality, and more specifically an association of shortened TL with Alzheimer’s disease, and are consistent with but not indicative of the possibility that TL may be a factor indicative of biological age," the authors conclude.
Source: medicalxpress.com
Yoga Reduces Stress; Now It’s Known Why
Six months ago, researchers at UCLA published a study that showed using a specific type of yoga to engage in a brief, simple daily meditation reduced the stress levels of people who care for those stricken by Alzheimer’s and dementia. Now they know why.
“The goal of the study was to determine if meditation might alter the activity of inflammatory and antiviral proteins that shape immune cell gene expression,” said Lavretsky. “Our analysis showed a reduced activity of those proteins linked directly to increased inflammation.
“This is encouraging news. Caregivers often don’t have the time, energy, or contacts that could bring them a little relief from the stress of taking care of a loved one with dementia, so practicing a brief form of yogic meditation, which is easy to learn, is a useful too.”
New drug could treat Alzheimer’s, multiple sclerosis and brain injury
July 24, 2012
A new class of drug developed at Northwestern University Feinberg School of Medicine shows early promise of being a one-size-fits-all therapy for Alzheimer’s disease, Parkinson’s disease, multiple sclerosis and traumatic brain injury by reducing inflammation in the brain.
Northwestern has recently been issued patents to cover this new drug class and has licensed the commercial development to a biotech company that has recently completed the first human Phase 1 clinical trial for the drug.
The drugs in this class target a particular type of brain inflammation, which is a common denominator in these neurological diseases and in traumatic brain injury and stroke. This brain inflammation, also called neuroinflammation, is increasingly believed to play a major role in the progressive damage characteristic of these chronic diseases and brain injuries.
By addressing brain inflammation, the new class of drugs — represented by MW151 and MW189 — offers an entirely different therapeutic approach to Alzheimer’s than current ones being tested to prevent the development of beta amyloid plaques in the brain. The plaques are an indicator of the disease but not a proven cause.
A new preclinical study published today in the Journal of Neuroscience, reports that when one of the new Northwestern drugs is given to a mouse genetically engineered to develop Alzheimer’s, it prevents the development of the full-blown disease. The study, from Northwestern’s Feinberg School and the University of Kentucky, identifies the optimal therapeutic time window for administering the drug, which is taken orally and easily crosses the blood-brain barrier.
"This could become part of a collection of drugs you could use to prevent the development of Alzheimer’s," said D. Martin Watterson, a professor of molecular pharmacology and biological chemistry at the Feinberg School, whose lab developed the drug. He is a coauthor of the study.
In previous animal studies, the same drug reduced the neurological damage caused by closed-head traumatic brain injury and inhibited the development of a multiple sclerosis-like disease. In these diseases as well as in Alzheimer’s, the studies show the therapy time window is critical.
How a Single Brain Trauma May Lead to Alzheimer’s Disease
ScienceDaily (July 24, 2012) — A study, performed in mice and utilizing post-mortem samples of brains from patients with Alzheimer’s disease, found that a single event of a moderate-to-severe traumatic brain injury (TBI) can disrupt proteins that regulate an enzyme associated with Alzheimer’s. The paper, published in The Journal of Neuroscience, identifies the complex mechanisms that result in a rapid and robust post-injury elevation of the enzyme, BACE1, in the brain. These results may lead to the development of a drug treatment that targets this mechanism to slow the progression of Alzheimer’s disease.
"A moderate-to-severe TBI, or head trauma, is one of the strongest environmental risk factors for Alzheimer’s disease. A serious TBI can lead to a dysfunction in the regulation of the enzyme BACE1. Elevations of this enzyme cause elevated levels of amyloid-beta, the key component of brain plaques associated with senility and Alzheimer’s disease," said first author Kendall Walker, PhD, postdoctoral associate in the department of neuroscience at Tufts University School of Medicine (TUSM).
Building on her previous work, neuroscientist Giuseppina Tesco, MD, PhD, of Tufts University School of Medicine (TUSM), led a research team that first used an in vivo model to determine how a single episode of TBI could alter the brain. In the acute phase (first two days) following injury, levels of two intracellular trafficking proteins (GGA1 and GGA3) were reduced, and an elevation of BACE1 enzyme level was observed.
Next, in an analysis of post-mortem brain samples from patients with Alzheimer’s disease, the researchers found that GGA1 and GGA3 levels were reduced while BACE1 levels were elevated in the brains of Alzheimer’s disease patients compared to the brains of people without Alzheimer’s disease, suggesting a possible inverse association.
In an additional experiment using a mouse strain genetically modified to express the reduced level of GGA3 that was observed in the brains of Alzheimer’s disease patients, the team found that one week following traumatic brain injury, BACE1 and amyloid-beta levels remained elevated even when GGA1 levels had returned to normal. The research suggests that reduced levels of GGA3 were solely responsible for the increase in BACE 1 levels and therefore the sustained amyloid-beta production observed in the sub-acute phase, or seven days, after injury.
"When the proteins are at normal levels, they work as a clean-up crew for the brain by regulating the removal of BACE1 enzymes and facilitating their transport to lysosomes within brain cells, an area of the cell that breaks down and removes excess cellular material. BACE1 enzyme levels may be stabilized when levels of the two proteins are low, likely caused by an interruption in the natural disposal process of the enzyme," said Tesco, assistant professor of neuroscience at Tufts School of Medicine and member of the neuroscience program faculty at the Sackler School of Graduate Biomedical Sciences at Tufts.
"We found that GGA1 and GGA3 act synergistically to regulate BACE1 post-injury. The identification of this interaction may provide a drug target to therapeutically regulate the BACE1 enzyme and reduce the deposition of amyloid-beta in Alzheimer’s patients," she continued. "Our next steps are to confirm these findings in post-mortem brain samples from patients with moderate-to-severe traumatic brain injuries."
Moderate-to-severe TBIs are caused most often by traumas, such as severe falls or motor vehicle accidents, that result in a loss of consciousness. Not all traumas to the head result in a TBI. According to the Centers for Disease Control and Prevention, each year 1.7 million people sustain a TBI. Concussions, the mildest form of a TBI, account for about 75% of all TBIs. Studies have linked repeated head trauma to brain disease and some previous studies have linked single events of brain trauma to brain disease, such as Alzheimer’s. Alzheimer’s disease currently affects as many as 5.1 million Americans and is the most common cause of dementia in adults age 65 and over.
Source: Science Daily
Brain discovery sheds light on link between vision and emotion
Neuroscientists have discovered a new area of the brain that is uniquely specialised for peripheral vision and could be targeted in future treatments for panic disorders and Alzheimer’s disease.
Published today in high impact journal Current Biology, researchers led by Dr Hsin-Hao Yu and Professor Marcello Rosa from Monash University’s Department of Physiology found that a brain area, known as prostriata, was specialised in detecting fast-moving objects in peripheral vision.
This area, located in a primitive part of the cerebral cortex, has characteristics unlike any other visual area described before, including a “direct line” of communication to brain areas controlling emotion and quick reactions.
Dr Yu said the discovery, identified during the development of the Monash Vision Group’s bionic eye, funded through the ARC Research in Bionic Vision Science and Technology Initiative, could lead to new treatments for panic disorders such as agoraphobia (fear of open spaces) and may extend into other medical areas including Alzheimer’s treatment.
“The brain is the most complex organ in the human body and perhaps the most remarkable. These findings change how we think of the brain in terms of how visual information is processed,” Dr Yu said.
“This area is likely to be hyperactive in panic disorder, with agoraphobia. This knowledge could lead to treatment options for the hyperactivity, and therefore sensitivity to such disorders, particularly the fear of open spaces.
“Correlation with previous studies also shows that prostriata is one of the first areas affected in Alzheimer’s disease. This knowledge helps to explain spatial disorientation and the tendency to fall, which are among the earliest signs of a problem associated with Alzheimer’s.”
Professor Rosa said this area had ultra-fast responses to visual stimuli, simultaneously broadcasting information to brain areas that control attention, emotional and motor reactions. This challenges current conceptions of how the brain processes visual information.
“This suggests a specialised brain circuit through which stimuli in peripheral vision can be fast-tracked to command quickly coordinated physical and emotional responses,” Professor Rosa said.
Music has big brain benefits compared to other leisure pursuits
Music rocks. Musical activity was found to preserve cognition, including memory, as you age, when comparing variability in cognitive outcomes of older adults active in musical instrumental and other leisure activities.
You won’t lose it if you don’t use it. A range of cognitive benefits including memory were sustained for musicians between the ages of 60-80 if they played for at least 10 years throughout their life, confirming the maintenance of advantages is not reliant on continued activity.
Start young. Timing of musical instrumental acquisition, before age nine, is important in optimizing cognitive benefits and was associated with enhanced verbal working memory functions.
It’s never too late, so keep at it. Sustained musical activity over the age of 60 was associated with other nonverbal cognitive benefits, and appeared to compensate for low educational attainment, which is possibly the greatest protection against age-related cognitive declines. This suggests that musical training should be considered an alternative form of education.
Anti-Tau Drug Improves Cognition, Decreases Tau Tangles in Alzheimer’s Disease Models
ScienceDaily (July 19, 2012) — While clinical trial results are being released regarding drugs intended to decrease amyloid production — thought to contribute to decline in Alzheimer’s disease — clinical trials of drugs targeting other disease proteins, such as tau, are in their initial phases.
Penn Medicine research presented July 19 at the 2012 Alzheimer’s Association International Conference (AAIC) shows that an anti-tau treatment called epithilone D (EpoD) was effective in preventing and intervening the progress of Alzheimer’s disease in animal models, improving neuron function and cognition, as well as decreasing tau pathology.
By targeting tau, the drug aims to stabilize microtubules, which help support and transport of essential nutrients and information between cells. When tau malfunctions, microtubules break and tau accumulates into tangles.
"This drug effectively hits a tau target by correcting tau loss of function, thereby stabilizing microtubules and offsetting the loss of tau due to its formation into neurofibrillary tangles in animal models, which suggests that this could be an important option to mediate tau function in Alzheimer’s and other tau-based neurodegenerative diseases," said John Trojanowski, MD, PhD, professor of Pathology and Laboratory Medicine in the Perelman School of Medicine at the University of Pennsylvania. "In addition to drugs targeting amyloid, which may not work in advanced Alzheimer’s disease, our hope is that this and other anti-tau drugs can be tested in people with Alzheimer’s disease to determine whether stabilizing microtubules damaged by malfunctioning tau protein may improve clinical and pathological outcomes."
The drug, identified through Penn’s Center for Neurodegenerative Disease Research (CNDR) Drug Discovery Program, was previously shown to prevent further neurological damage and improve cognitive performance in animal models*. The Penn research team includes senior investigator Bin Zhang, MD, and Kurt Brunden, PhD, director of Drug Discovery at CNDR.
Bristol-Myers Squibb, who developed and owns the rights to the drug, has started enrolling patients into a phase I clinical trial in people with mild Alzheimer’s disease.
Source: Science Daily
Alzheimer’s disease linked to diabetes, study suggests
ScienceDaily (July 18, 2012) — Researchers from the University of Medicine and Dentistry of New Jersey (UMDNJ), collaborating with scientists from Northwestern University in Illinois, have provided direct experimental evidence that diabetes is linked to the onset of Alzheimer’s disease. The study, published online this week in the Journal of Alzheimer’s Disease, used an experimental model that shows potential as an important new tool for investigations of Alzheimer’s disease and of drugs being developed to treat Alzheimer’s.
UMDNJ researchers Peter Frederikse, PhD, and Chinnaswamy Kasinathan, PhD, collaborated with William Klein, PhD, at Northwestern University, to build on prior studies from the Klein lab and others that indicated close links between Alzheimer’s disease and diabetes. Working with Claudine Bitel and Rajesh Kaswala, students at UMDNJ, the researchers tested whether untreated diabetes would provide a physiological model of Alzheimer neuropathology.
"The results were striking," Frederikse said. "Because we used diabetes as an instigator of the disease, our study shows — for the first time directly — the link between Alzheimer’s and diabetes."
The researchers found substantial increases in amyloid beta peptide pathology — a hallmark of Alzheimer’s disease — in the brain cortex and hippocampus concurrent with diabetes. They also found significant amyloid beta pathology in the retina and by contrast, when diabetes is not present, no observable pathology was detected in either the brain or the retina.
"Second, our study examined the retina, which is considered an extension of the brain, and is more accessible for diagnostic exams," Frederikse added. "Our findings indicate that scientists may be able to follow the onset and progression of Alzheimer’s disease through retinal examination, which could provide a long sought after early-warning sign of the disease."
This experimental model replicated spontaneous formation of amyloid beta “oligomer” assemblies in brain and retina which may help to explain one of the most widely recognized symptoms of Alzheimer’s. “This is exciting,” Klein said. “Oligomers are the neurotoxins now regarded as causing Alzheimer’s disease memory loss. What could cause them to appear and buildup in late-onset Alzheimer’s disease has been a mystery, so these new findings with diabetes represent an important step.”
Previous research indicated that insulin plays an important role in the formation of memories. Once attached to neurons, oligomers cause insulin receptors to be eliminated from the surface membranes, contributing to insulin resistance in the brain. This launches a vicious cycle in which diabetes induces oligomer accumulation which makes neurons even more insulin resistant.
"In light of the near epidemic increases in Alzheimer’s disease and diabetes today, developing a physiological model of Alzheimer neuropathology has been an important goal," Kasinathan added. "It allows us to identify a potential biomarker for Alzheimer’s disease and may also make important contributions to Alzheimer drug testing and development."
Source: Science Daily