Alzheimer protease hitches a ride
Article Abstract:
A study suggests that activation of certain G protein-coupled receptors stimulates production of the neurotoxic amyloid-[beta] peptide through internalization of a membrane-embedded protease. The findings emphasize the role of the [[beta].sub.2]-adrenergic receptor and suggest that blocking this stress-related signaling pathway might reduce the risk of Alzheimer disease.
Publication Name: Nature Medicine
Subject: Health
ISSN: 1078-8956
Year: 2006
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PrPSc accumulation in myocytes from sheep incubating natural scrapie
Article Abstract:
Scrapie-affected sheep accumulate the prion protein PrPSc in a myocyte subset, both experimentally and naturally. Small amounts of PrPSc in sheep muscle do not alter the human transmission risk, as lymph modes can bear a reasonably higher PrPSc load.
Publication Name: Nature Medicine
Subject: Health
ISSN: 1078-8956
Year: 2004
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Does Alzheimer disease tilt the scales of amyloid degradation versus accumulation?
Article Abstract:
Alzheimer's disease and other neurodegenerative diseases may be caused by a deficiency of a protease called neprilysin. This protease degrades amyloid beta-peptide, which accumulates in abnormal amounts in the brains of Alzheimer's patients.
Publication Name: Nature Medicine
Subject: Health
ISSN: 1078-8956
Year: 2000
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