Alzheimer's disease (AD) is the most common type of senile dementia, characterized by
neurofibrillary tangle and amyloid plaque in brain pathology. Major efforts in AD drug were …

In the 12 years since the publication of the first Consensus Paper of the WFSBP on
biomarkers of neurodegenerative dementias, enormous advancement has taken place in …

Signalling through the receptor protein Notch, which is involved in crucial cell-fate decisions
during development, requires ligand-induced cleavage of Notch. This cleavage occurs …

Point mutations in the presenilin-1 gene (PS1) are a major cause of familial Alzheimer's
disease. They result in a selective increase in the production of the amyloidogenic peptide …

Various mutations in the amyloid protein precursor and presenilin genes can lead to early
onset, autosomal Alzheimer's disease. A series of mis-sense mutations (with one exception) …

It is a truism of modern biomedical science that the development of therapies expected to
slow or arrest the progression of a disease requires as detailed an understanding of its …

Dominantly inherited mutations in the genes encoding presenilins (PS) and the amyloid
precursor protein (APP) are the major causes of familial Alzheimer's disease (AD). The …

The release of amyloidogenic amyloid-β peptide (Aβ) from amyloid-β precursor protein
(APP) requires cleavage by β-and γ-secretases. In contrast, α-secretase cleaves APP within …

Aggregation and fibril formation of amyloid-β (Aβ) peptides Aβ40 and Aβ42 are central
events in the pathogenesis of Alzheimer disease. Previous studies have established the …

Progressive cerebral amyloid β-protein (Aβ) deposition is believed to play a central role in
the pathogenesis of Alzheimer's disease (AD). Elevated levels of Aβ (42) peptide formation …