Abstract

Alzheimer disease (AD), which is associated with chronic and progressive neurodegeneration, is the most prevalent cause of dementia linked to aging. Among the risk factors for AD, age stands as the greatest one, with the vast majority of people with AD being 65 years of age or older. Nevertheless, the pathophysiologic mechanisms underlying the link between aging and the development of AD, although not completely understood, might reveal important aspects for the understanding of this pathology. Thus, there is significant evidence that the impaired thermal homeostasis associated with normal aging leads to a variety of metabolic changes that could be associated with AD development. In this chapter, we assess the clinical and biochemical evidence implicating hypothermia as a risk factor for the development of AD and the impact of hypothermia on the two pathologic hallmarks of AD: accumulation of senile plaques of amyloid-beta and neurofibrillary tangles of aberrant hyperphosphorylated tau protein.

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