The neuropathological hallmarks of Alzheimer's disease include extracellular neuritic
plaques and neurofibrillary tangles. The neuritic plaques contain β-amyloid peptides (Aβ …

Amyloid-β (Aβ) peptides, 36–43 amino acids in length, are produced from β-and γ-secretase
cleavage of the amyloid-β protein precursor (AβPP), and are one of the causative agents of …

N‐terminally truncated amyloid‐β (Aβ) peptides are present in early and diffuse plaques of
individuals with Alzheimer's disease (AD), are overproduced in early onset familial AD and …

That the topography, severity, and progression of β-amyloid deposition in the brain of
Alzheimer's disease (AD) and Down's syndrome (DS) cases is not uniform is well …

Although N-truncated Aβ variants are known to be the main constituent of amyloid plaques
in the brains of patients with Alzheimer's disease, their potential as targets for …

We measured tissue distribution and expression pattern of the beta‐site amyloid precursor
protein (APP)‐cleaving enzyme (BACE) in the brains of transgenic Tg2576 mice that show …

To study amyloid β‐protein (Aβ) production and aggregation in vivo, we created two
transgenic (Tg) mouse lines expressing the C‐terminal 100 amino acids of human amyloid …

Evidence for a central role of amyloid β-protein (Aβ) in the genesis of Alzheimer's disease
(AD) has led to advanced human trials of Aβ-lowering agents. The “amyloid hypothesis” of …

Extracellular and intraneuronal accumulation of amyloid-beta (Aβ) peptide aggregates in the
brain has been hypothesized to play an important role in the neuropathology of Alzheimer's …

Insoluble pools of the amyloid-β peptide (Aβ) in brains of Alzheimer's disease patients
exhibit considerable N-and C-terminal heterogeneity. Mounting evidence suggests that both …