title: Hypothermia and Alzheimer's disease neuropathogenic pathways.
abstract: Alzheimer's disease (AD) remains a major health problem, and accounts for 50 to 60% of all cases of dementia. The two histopathological hallmarks of AD are senile plaques, composed of the β-amyloid peptide (Aβ), and intraneuronal neurofibrillary tangles composed of abnormally hyperphosphorylated tau protein. Only a small proportion of AD is due to mutations in the genome of patients, the large majority of cases being of late onset and sporadic in origin. The relative contribution of genetics and environment to the sporadic cases is unclear, but they are accepted to be of multifactorial origin. This means that genetic and environmental factors can interact together to induce or accelerate the disease. Among environmental factors, studies suggest that hypothermia may contribute to the development and exacerbation AD. Here, we review the preclinical data involving hypothermia with tau and Aβ, as well as clinical evidence implicating hypothermia in the development of AD.
authors.affiliation: Department of Anesthesiology, College of Physicians and Surgeons, Columbia University, 622 West 168th Street PH 5, New York, NY 10032, USA.
authors.forename: R A
authors.initials: RA
authors.lastname: Whittington
authors.forename: M-A
authors.initials: MA
authors.lastname: Papon
authors.forename: F
authors.initials: F
authors.lastname: Chouinard
authors.forename: E
authors.initials: E
authors.lastname: Planel
mesh_terms: D000544:Alzheimer Disease / Q000209:etiology* / Q000378:metabolism / Q000473:pathology*; D016229:Amyloid beta-Peptides / Q000502:physiology; D000818:Animals; D006801:Humans; D007035:Hypothermia / Q000209:etiology* / Q000378:metabolism / Q000473:pathology*; D015398:Signal Transduction / Q000502:physiology*; D016875:tau Proteins / Q000502:physiology
chemical_list: D016229:Amyloid beta-Peptides; C054369:MAPT protein, human; D016875:tau Proteins