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Alzheimer's disease is believed to occur when abnormal amounts of amyloid beta (Aβ), accumulating extracellularly as amyloid plaques and tau proteins, or intracellularly as neurofibrillary tangles, form in the brain, affecting neuronal functioning and connectivity, resulting in a progressive loss of brain function.[40][41] This altered protein clearance ability is age-related, regulated by brain cholesterol,[42] and associated with other neurodegenerative diseases.[43][44]

The cause for most Alzheimer's cases is still mostly unknown,[9] except for 1–2% of cases where deterministic genetic differences have been identified.[13] Several competing hypotheses attempt to explain the underlying cause; the most predominant hypothesis is the amyloid beta (Aβ) hypothesis.[9]