A central question in Alzheimer's disease (AD) research is what role β-amyloid peptide (Aβ)
plays in synaptic dysfunction. Synaptic activity increases Aβ secretion, potentially inhibiting …

A local increase in amyloid-β peptide (Aβ) is closely associated with synaptic dysfunction in
the brain in Alzheimer's disease. Here, we report on the catabolic mechanism of Aβ at the …

A central question in Alzheimer's disease research is what role synaptic activity plays in the
disease process. Synaptic activity has been shown to induce β-amyloid peptide release into …

The accumulation of amyloid-β (Aβ) peptides in the brain of patients with Alzheimer's
disease (AD) may arise from an imbalance between Aβ production and clearance …

A subtle but chronic alteration in metabolic balance between amyloid-β peptide (Aβ)
anabolic and catabolic activities is thought to cause Aβ accumulation, leading to a decade …

Abnormally high concentrations of β-amyloid peptide (Aβ) and amyloid plaque formation in
Alzheimer's disease (AD) may be caused either by increased generation or by decreased …

The amyloid-β42 (Aβ42) peptide has been suggested to play a causative role in Alzheimer
disease (AD). Neprilysin (NEP) is one of the rate-limiting Aβ-degrading enzymes, and its …

The deposition of amyloid-beta peptide (Abeta) causes the long-term pathological cascade
of Alzheimer's disease (AD). Neprilysin is a rate-limiting peptidase, which participates in …

Converging evidence suggests that the accumulation of cerebral amyloid β-protein (Aβ) in
Alzheimer's disease (AD) reflects an imbalance between the production and degradation of …

The accumulation of the β-amyloid peptide (Aβ) in Alzheimer's disease (AD) is thought to
play a causative role in triggering synaptic dysfunction in neurons, leading to their eventual …