Results 181 to 190 of about 40,397 (225)

Presenilin-1 mutations in Alzheimer's disease

Nature, 2000
Mutations in the gene encoding the protein presenilin-1 are the most common cause of familial Alzheimer's disease1 and they often produce a different disease course from sporadic Alzheimer's and another familial form associated with mutations in the gene encoding β-amyloid precursor protein2.
RUSSO, Claudio   +9 more
openaire   +6 more sources

Two transmembrane aspartates in presenilin-1 required for presenilin endoproteolysis and γ-secretase activity

Nature, 1999
Accumulation of the amyloid-beta protein (Abeta) in the cerebral cortex is an early and invariant event in the pathogenesis of Alzheimer's disease. The final step in the generation of Abeta from the beta-amyloid precursor protein is an apparently intramembranous proteolysis by the elusive gamma-secretase(s).
M S, Wolfe   +5 more
openaire   +4 more sources

Presenilin-1 in Neuroblastoma Cells

Toxicology in Vitro, 1998
Presenilin-1 expression was investigated in Neuro-2a cells using the alphaPS1Loop antibody. The bulk of the immunoreactivity was found as the approximately 18kDa C-terminal fragment. Hydrogen peroxide treatment of the Neuro-2a cells for 24 hours resulted in a concentration-dependent cytotoxicity with a critical concentration of hydrogen peroxide of ...
C, Lindblad   +3 more
openaire   +2 more sources

Regulation of Apoptosis by Presenilin 1

Neurobiology of Aging, 1998
Familial Alzheimer's disease is transmitted as an autosomal dominant disorder and, in 5-10% of the cases, is caused by mutations in the coding regions of two homologous genes, Presenilin 1 and 2 (PS1 and PS2). Previously, we have shown that PS2, a homolog of PS1.
B, Wolozin, P, Alexander, J, Palacino
openaire   +2 more sources

Presenilin-1 expression in Pick's disease

Acta Neuropathologica, 1999
Recent studies have reported that neuronal populations expressing low levels of presenilin-1 (PS-1) display increased vulnerability in late-onset sporadic Alzheimer's disease (AD). To examine whether this phenomenon also occurs in other neurodegenerative diseases, we performed a quantitative immunocytochemical study of PS-1 distribution in the cerebral
P, Giannakopoulos   +6 more
openaire   +2 more sources

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