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Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein
ALZHEIMER'S disease (AD) is the most common cause of progressive intellectual failure in aged humans. AD brains contain numerous amyloid plaques surrounded by dystrophic neurites, and show profoundExpand
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Peripherally administered antibodies against amyloid β-peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer disease
One hallmark of Alzheimer disease is the accumulation of amyloid β-peptide in the brain and its deposition as plaques. Mice transgenic for an amyloid β precursor protein (APP) mini-gene driven by aExpand
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Immunization with amyloid-β attenuates Alzheimer-disease-like pathology in the PDAPP mouse
Amyloid-β peptide (Aβ) seems to have a central role in the neuropathology of Alzheimer's disease (AD). Familial forms of the disease have been linked to mutations in the amyloid precursor proteinExpand
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Purification and cloning of amyloid precursor protein β-secretase from human brain
Proteolytic processing of the amyloid precursor protein (APP) generates amyloid β (Aβ) peptide, which is thought to be causal for the pathology and subsequent cognitive decline in Alzheimer'sExpand
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Phosphorylation of Ser-129 Is the Dominant Pathological Modification of α-Synuclein in Familial and Sporadic Lewy Body Disease*
A comprehensive, unbiased inventory of synuclein forms present in Lewy bodies from patients with dementia with Lewy bodies was carried out using two-dimensional immunoblot analysis, novel sandwichExpand
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Isolation and quantification of soluble Alzheimer's β-peptide from biological fluids
CEREBRAL deposition of the β-amyloid peptide (Aβ) is an invariant feature of Alzheimer's disease. Since the original isola-tion and characterization of αβ (ref. 1) and the subsequent cloning of itsExpand
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Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid β-protein in both transfected cells and transgenic mice
The mechanism by which mutations in the presenilin (PS) genes cause the most aggressive form of early-onset Alzheimer's disease (AD) is unknown, but fibroblasts from mutation carriers secreteExpand
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Mutation of the β-amyloid precursor protein in familial Alzheimer's disease increases β-protein production
PROGRESSIVE cerebral deposition of the 39–43-amino-acid amy-loid β-protein (Aβ) is an invariant feature of Alzheimer's disease which precedes symptoms of dementia by years or decades. The onlyExpand
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Mutation of the beta-amyloid precursor protein in familial Alzheimer's disease increases beta-protein production.
Progressive cerebral deposition of the 39-43-amino-acid amyloid beta-protein (A beta) is an invariant feature of Alzheimer's disease which precedes symptoms of dementia by years or decades. The onlyExpand
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Amyloid precursor protein processing and A beta42 deposition in a transgenic mouse model of Alzheimer disease.
The PDAPP transgenic mouse, which overexpresses human amyloid precursor protein (APP717V-->F), has been shown to develop much of the pathology associated with Alzheimer disease. In this report,Expand
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