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Dr. Manuel Montero-Odasso, a Lawson scientist, geriatrician at St. Joseph's Health Care London, and associate professor in the Division of Geriatric Medicine at Western University's Schulich School of Medicine & Dentistry, is leading the "Gait and Brain Study." His team is assessing up to 150 seniors with mild cognitive impairment (MCI), a slight decline of memory and other mental functions which is considered a pre-dementia syndrome, in order to detect an early predictor of cognitive and mobility decline and progression to dementia. "Finding methods to detect dementia early is vital to our ability to slow or halt the progression of the disease," says Dr. Montero-Odasso. The study, funded by the Canadian Institutes of Health Research, followed participants for six years and included bi-annual visits. Researchers asked participants to walk while simultaneously performing a cognitively demanding task, such as counting backwards or naming animals. Those...

Auriel Willette, an ISU assistant professor of food science and human nutrition who led the study, says the researcher who initially discovered the gene, TOMM40 (Translocase of Outer Mitochondrial Membrane-40kD), found it increased the risk for Alzheimer's. However, when multiple studies failed to replicate the results, many researchers dismissed the findings, Willette said. Not convinced the gene was a total bust, Willette decided to look at other factors that may be contributing to the mixed results. In the paper published online by  Alzheimer's & Dementia : The Journal of the Alzheimer's Association as an in press corrected proof, Willette and his colleagues found a dramatic difference in the gene's impact on memory, general cognitive function and risk based on a family history of Alzheimer's disease and the length of a specific section of the gene. "It was kind of a shot in the dark, but we found if you don't have a family history of Alzheimer...

The finding potentially could explain the mechanism by which Alzheimer's, Parkinson's, Huntington's, and other neurodegenerative diseases spread within the brain and disrupt normal brain functions. The finding also suggests that an effective treatment  for one neurodegenerative disease might work for other neurodegenerative diseases as well. The study by senior author Edward Campbell, PhD, first author William Flavin, PhD, and colleagues is published in the journal  Acta Neuropathologica . "A possible therapy would involve boosting a brain cell's ability to degrade a clump of proteins and damaged vesicles," Campbell said. "If we could do this in one disease, it's a good bet the therapy would be effective in the other two diseases." Neurodegenerative diseases are caused by the death of neurons and other cells in the brain, with different diseases affecting different regions of the brain. Alzheimer's destroys memory, while Parkinson...

ALS, also known as Lou Gehrig's disease, is a lethal, progressive neurodegenerative disorder that affects the motor nerve cells in both the brain and the spinal cord. The progressive degeneration of motor neurons leads to atrophy, paralysis and eventually death due to failure of the respiratory muscles. Since the exact cause of ALS is unknown, current research has focused on extending the post-onset life expectancy, which is currently between two to five years for most patients. Part of the disease's progression is linked to increased activity of glial cells, a type of immune cell that damages and kills the body's motor neuron cells and decreases their ability to cleanse the CNS environment. Dr. Rachel Lichtenstein of the Avram and Stella Goldstein-Goren Department of Biotechnology Engineering at BGU has focused on reducing this negative immune response. "We found a way to thwart the glial cells from attacking and killing healthy brain cells," says Dr. Lic...

The findings, which appear in the journal  eLife , may one day lead to better therapies and treatments for these diseases. The prion protein plays a crucial role in fatal neurodegenerative  disorders like Creutzfeldt-Jakob disease in humans and "mad cow disease" in cattle. Prion diseases are part of larger group of human neurodegenerative disorders, including Alzheimer's, Parkinson's and Huntington's diseases, which are all due to the abnormal accumulation of protein aggregates in the brain. According to the researchers, how nerve cells are damaged in these diseases has remained a mystery until now. "Our work shows that the prion protein acts like a molecular on-off switch. In the "on" positon, one end of the protein delivers a toxic signal to nerve cells, while in the "off" position, the other end of the protein serves as a brake to reduce the toxic signal. Moreover, copper, a metal that is a normal component of brain biochemistry, ...

Every day billions of people across the planet successfully navigate their environments, for example when they go to work or head home. Such journeys generally happen with little conscious effort and rest on the brain's ability to use overall knowledge of an environment to make estimates of where it finds itself. The ability to make fine grained assessments of location is seated in the hippocampus, a seahorse-shaped structure located in the temporal lobe. Research shows that the precise mechanism for navigation includes hippocampal place cells, which increase or decrease in electrical activity depending on one's location. However, when making their daily commute, people don't need very detailed representations of which houses they pass in which order. Instead, they can make due with more course information. Left at the museum and somewhere down the road right again at the supermarket, called topographical orientation. Building on current research, the researchers invest...

"In the last decade or so, there has been a lot of work on biomarkers for early Alzheimer's disease," Han says. "There are new imaging methods that can identify neuropathological brain changes that happen early on in the course of the disease. The problem is that they are not widely available, can be invasive and are incredibly expensive. I wanted to see whether the cognitive tests I regularly use as a neuropsychologist relate to these biomarkers." Putting neuropsychological measures to the test Han and his colleagues conducted a meta-analysis of 61 studies to explore whether neuropsychological tests can identify early Alzheimer's disease in adults over 50 with normal cognition. The study, which was published in  Neuropsychology Review , found that people who had amyloid plaques performed worse on neuropsychological tests of global cognitive function, memory, language, visuospatial ability, processing speed and attention/working memory/executive funct...

The discovery has been years in the making. Back in 2012, Katherine Duncan used functional magnetic resonance imaging (fMRI) to identify how the brain triggers memory states, uncovering a brain region that detects novelty. She then demonstrated that novelty detection acts like a switch, changing how the brain learns and remembers. Finally, she determined the impact of novelty on human memory. As she puts it, "We find that familiarity increased retrieval of other unrelated memories but reduced the chances for memory formation. On the other hand, novelty enhanced the later formation of distinct memories without worrying about previous experiences." Duncan suggests we need to revisit how we make memories. "Your ability to remember something doesn't just depend on the strength of the memory, it depends on the state that you're in." Her work also hints at new strategies to improve memory development. "We're using what we know about the brain to deve...

Salk and UC San Diego scientists performed an enormous survey of microglia (pictured right here), revealing hyperlinks to neurodegenerative illnesses and psychiatric diseases. Credit score: Nicole Coufal Scientists have, for the primary time, characterised the molecular markers that make the mind's entrance strains of immune protection -- cells referred to as microglia -- distinctive. Within the course of, they found additional proof that microglia might play roles in a wide range of neurodegenerative and psychiatric diseases, together with Alzheimer's, Parkinson's and Huntington's illnesses in addition to schizophrenia, autism and melancholy. "Microglia are the immune cells of the mind, however how they operate within the human mind just isn't effectively understood," says Rusty Gage, professor in Salk's Laboratory of Genetics, the Vi and John Adler Chair for Analysis on Age-Ass...

"Through this study, members of the Down syndrome community have demonstrated loudly and clearly that they are eager to participate in clinical  trials, particularly studies that provide promise for the treatment of Alzheimer's disease," says Brian Skotko, MD, MPP, co-director of the Massachusetts General Hospital (MGH) Down Syndrome Program, and a site principal investigator for the trial. "This first, industry-sponsored phase 2 trial in the Down syndrome community showed that people with Down syndrome were able to follow the study protocol and that the drug was safe and tolerable." The most common form of intellectual disability in the United States, Down syndrome is caused by an extra copy of chromosome 21. People with Down syndrome exhibit various degrees of intellectual disability and are at greatly increased risk of developing Alzheimer's dementia as they age. Excess activity of the genes on chromosome 21 -- including the gene for the amyloid prec...