Chronic, progressive neurodegenerative disorder characterized by a global, nonreversible impairment in cerebral functioning. Deteriorating course over up to 8-10 years.
Brain lesions are marked by neurofibrillary tangles, senile plaques, neuronal loss, and brain atrophy, with defects in acetylcholine synthesis at the cellular level.
The ultimate neurotoxin in<unk>  is debated, but experimental evidence highlights small aggregates of amyloid beta peptides called oligomers, as opposed to larger aggregates called fibril
Pathogenesis of<unk>  also involves a second protein, tau. The accumulation of this altered protein is toxic to neurons in experimental models.
There are three alleles of APOE, called epsilon 2 (e2), e3, and e4, and their encoded isoforms also vary in several activities. One mechanism by which inheritance of the APOE e4 may increase<unk>  risk is by impairing amyloid beta clearance from cerebrum
Dementia pathophysiology
Parkinson's disease pathophysiology
Amnesia pathophysiology
Schizophrenia pathophysiology
Personality disorder pathophysiology
Lesch-Nyhan syndrome pathophysiology
Anhedonia pathophysiology
Asperger syndrome pathophysiology