Although extensive data support a central pathogenic role for amyloid β protein (Aβ) in
Alzheimer's disease 1 , the amyloid hypothesis remains controversial, in part because a specific …

Alzheimer's disease is characterized by extensive cerebral amyloid deposition. Amyloid
deposits associated with damaged neuropil and blood vessels contain abundant fibrils formed …

Alzheimer's disease constitutes a rising threat to public health. Despite extensive research
in cellular and animal models, identifying the pathogenic agent present in the human brain …

Converging lines of evidence suggest that progressive accumulation of the amyloid β‐protein
(Aβ) plays a central role in the genesis of Alzheimer’s disease, but it was long assumed …

A central unresolved problem in research on Alzheimer disease is the nature of the molecular
entity causing dementia. Here we provide the first direct experimental evidence that a …

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that is thought to be
caused in part by the age-related accumulation of amyloid β-protein (Aβ). The presence of …

Alzheimer's disease (AD) is characterized by decreased synapse density in hippocampus
and neocortex, and synapse loss is the strongest anatomical correlate of the degree of clinical …

Acutely developing lesions of the brain have been highly instructive in elucidating the neural
systems underlying memory in humans and animal models. Much less has been learned …

Fibrillogenesis of the amyloid β-protein (Aβ) is a seminal pathogenetic event in Alzheimer's
disease. Inhibiting fibrillogenesis is thus one approach toward disease therapy. Rational …

In Alzheimer's disease (AD), the impairment of declarative memory coincides with the
accumulation of extracellular amyloid-β protein (Aβ) and intraneuronal tau aggregates. Dementia …