beta-Amyloid precursor protein (beta-APP), the source of the fibrillogenic amyloid beta-
peptide (A beta) that accumulates in the brain of victims of Alzheimer's disease, is a …

Since the identification of tau as the main component of neurofibrillary tangles in Alzheimer's
disease and related tauopathies, and the discovery that mutations in the tau gene cause …

Aβ1–42 is a self-associating peptide whose neurotoxic derivatives are thought to play a role
in Alzheimer's pathogenesis. Neurotoxicity of amyloid β protein (Aβ) has been attributed to …

Over the past several years, experiments with synthetic amyloid-beta peptide (Aβ) and
animal models have strongly suggested that pathogenesis of Alzheimer's disease (AD) …

Alzheimer's disease (AD) is characterized by presence of extracellular fibrillar Aβ in amyloid
plaques, intraneuronal neurofibrillary tangles consisting of aggregated hyperphosphorylated …

Accumulation of advanced glycation endproducts (AGE) in the brain is a feature of ageing
and degeneration, especially in Alzheimer's disease (AD). Increased AGE levels explain …

Previous studies have implicated the failure to degrade aggregated Aβ1‐42 in late
endosomes or secondary lysosomes as a mechanism for the accumulation of β‐amyloid in …

The cause of neuronal degeneration in Alzheimer's disease (AD) has not been completely
clarified, but has been variously attributed to increases in cytosolic calcium and increased …

The oligomer hypothesis for Alzheimer's disease (AD) was introduced in 1998. It was based
on evidence that oligomers could exist free of amyloid fibrils, that fibril-free oligomer …

Retinoic acid (RA) induces the differentiation of many cell lines, including those derived from
neuroblastoma. RA treatment of SH‐SY5Y cells induces the appearance of functional Trk B …