http://www.nytimes.com/2014/03/20/health/fetal-gene-may-protect-brain-from-alzheimers-study-finds.html?
It
is one of the big scientific mysteries of Alzheimer’s disease: Why do
some people whose brains accumulate the plaques and tangles so strongly
associated with Alzheimer’s not develop the disease?
Now,
a series of studies by Harvard scientists suggests a possible answer,
one that could lead to new treatments if confirmed by other research.
The
memory and thinking problems of Alzheimer’s disease and other
dementias, which affect an estimated seven million Americans, may be
related to a failure in the brain’s stress response system, the new
research suggests. If this system is working well, it can protect the
brain from abnormal Alzheimer’s proteins; if it gets derailed, critical
areas of the brain start degenerating.
The rest is at the link behind the NYTimes paywall.
Abstract here;
REST and stress resistance in aging and Alzheimer’s disease
Article preview View full access options
- Nature
- doi:10.1038/nature13163
- Received
- Accepted
- Published online
Abstract
Human neurons are functional over an entire lifetime, yet the mechanisms that preserve function and protect against neurodegeneration during ageing are unknown. Here we show that induction of the repressor element 1-silencing transcription factor (REST; also known as neuron-restrictive silencer factor, NRSF) is a universal feature of normal ageing in human cortical and hippocampal neurons. REST is lost, however, in mild cognitive impairment and Alzheimer’s disease. Chromatin immunoprecipitation with deep sequencing and expression analysis show that REST represses genes that promote cell death and Alzheimer’s disease pathology, and induces the expression of stress response genes. Moreover, REST potently protects neurons from oxidative stress and amyloid β-protein toxicity, and conditional deletion of REST in the mouse brain leads to age-related neurodegeneration. A functional orthologue of REST, Caenorhabditis elegans SPR-4, also protects against oxidative stress and amyloid β-protein toxicity. During normal ageing, REST is induced in part by cell non-autonomous Wnt signalling. However, in Alzheimer’s disease, frontotemporal dementia and dementia with Lewy bodies, REST is lost from the nucleus and appears in autophagosomes together with pathological misfolded proteins. Finally, REST levels during ageing are closely correlated with cognitive preservation and longevity. Thus, the activation state of REST may distinguish neuroprotection from neurodegeneration in the ageing brain.
What is your doctor doing to make sure your 33% chance of getting dementia/Alzheimers post stroke is avoided?
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