Amyloid Deposits in Cognitively Normal People May Predict Risk for Alzheimer’s Disease

For people free of dementia, abnormal deposits of a protein associated with Alzheimer’s disease are associated with increased risk of developing the symptoms of the progressive brain disorder, according to two studies from researchers at Washington University in St. Louis. The studies, primarily funded by the National Institute on Aging (NIA), part of the National Institutes of Health, linked higher amounts of the protein deposits in dementia-free people with greater risk for developing the disease, and with loss of brain volume and subtle declines in cognitive abilities.

Normal brain vs. Alzheimers brain

Book Review: The SharpBrains Guide to Brain Fitness

Many people believe that the brain is hardwired in childhood and, as we grow older, cognitive decline is inevitable; we becoming more forgetful, less inclined to seek new experiences and more set in our ways. During the late 1990s, the work of early childhood advocates to focus on learning during the first three years of life had a dramatic impact public opinion and social policy that has lasted almost a decade. Indeed, the importance of learning during a child’s first three years of life was widely accepted as a fact of early neurological development. Unfortunately, advocacy efforts actually countered what neuroscientists were discovering about the brain and its development [1].

Scientific research in the late 1990s was finding that the adult brain had a much greater capacity for neuroplasticity — the ability to change structure and function in response to thought, learning and experience — than was previously believed [2-3]. Neuroscientists found that the adult brain was capable of growing new dendrites, branched projections from a neuron or nerve cell that conduct electrochemical stimulation received from other neural cells toward the cell body of the neuron, which are often damaged as a result of traumatic head injury or stroke. In adult macaques, researchers found that new neurons were produced in brain regions important for congitive function [4]. The view that aging was equivalent to ubiquitous and rapid cognitive decline thus gave way to a recognition that, for some people, mental acuity continues well into old age. Today, it’s common to hear about “brain fitness” and/or “brain training” products that can help to maintain and/or rebuild cognitive performance. However, in this rapidly evolving field, it’s difficult to discern fact from fiction.

Health Highlights – September 8th, 2009

Health Highlights is a biweekly summary of particularly interesting articles from credible sources of health and medical information that we follow & read. For a complete list of recommeded sources, see our links page.

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Metabolic Changes in Human Brain Evolution and Schizophrenia

Earlier this year, researchers at the Max Plank Institute for Evolutionary Anthropology, the Shanghai branch of the Chinese Academy of Sciences and Cambridge University published a study in the journal Genome Biology providing further evidence that the evolution of human cognitive abilities was accompanied by adaptive changes in brain metabolism, potentially pushing the human brain to the limit of its metabolic capabilities [1]. The results support the theory that schizophrenia is a consequence of human brain evolution.

Neurodegenerative Disease and the Coming Epidemic

At Neuroscience 2008, the 38th annual meeting of the Society for Neuroscience held last month in Washington D.C., a number of researchers presented evidence that a small, soluble, clustered form of a protein called amyloid beta may be responsible for brain damage in Alzheimer’s disease patients [1]. In addition, scientists report that they are finding new sources and uses of neural stem cells that may replace cells damaged by neurodegenerative disorders such as Alzheimer’s and Parkinson’s disease [2].

Creative Commons License photo credit: neurollero

Why are these reports significant? Because until recently, large insoluble amyloid beta plaques, or deposits, were considered the likely cause of Alzheimer’s disease. The plaques were thought to disrupt brain cell communication. However, new findings show that an early (i.e. small), soluble, clustered form of amyloid beta called protofibrils is found in high levels in the brains of people with Alzheimer’s disease [1]. Researchers also found a strong correlation between the presence of high levels of protofibrils in the brains of transgenic mouse models of Alzheimer’s disease and the cognitive impairments associated with the disease.