Abstract
Alzheimer’s disease (AD) is characterized histopathologically by neurodegeneration associated with numerous extracellular Abeta plaques and intraneuronal neurofibrillary tangles of hyperphosphorylated tau. Although studies have implicated both Aβ and tau pathologies in causing cognitive impairment, neurodegeneration, which accounts for the loss of brain mass to the tune of 200-300 g over the average disease progression of 7-10 years, is the most proximal pathology to the development of dementia in AD patients. Substantial evidence suggests that the Aβ and hyperphosphorylated tau (ptau) oligomers, rather than Aβ plaques and tau neurofibrillary tangles (NFTs), are the primary cause of neurodegeneration and dementia.
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