The role of Aβ42 in Alzheimer's diseaseRôle de l'Aβ42 dans la maladie d'Alzheimer
References (32)
- et al.
Familial Alzheimer's disease-linked presenilin 1 variants elevate Aβ1-42/1-40 ratio in vitro and in vivo
Neuron
(1996) - et al.
Alzheimer's disease: initial report of the purification and characterization of a novel cerebrovascular amyloid protein
Biochem. Biophys. Res. Commun.
(1984) - et al.
Visualization of A beta 42 (43) and A beta 40 in senile plaques with end-specific A beta monoclonals: evidence that an initially deposited species is A beta 42 (43)
Neuron
(1994) - et al.
Mass spectrometry of purified amyloid beta protein in Alzheimer's disease
J. Biol. Chem.
(1992) - et al.
Release of excess amyloid beta protein from a mutant amyloid beta protein precursor
Science
(1993) - et al.
Early-onset Alzheimer's disease caused by mutations at codon 717 of the beta-amyloid precursor protein gene
Nature
(1991) - et al.
Mutation of the beta-amyloid precursor protein in familial Alzheimer's disease increase beta-protein production
Nature
(1992) - et al.
Excessive production of amyloid beta-protein by peripheral cells of symptomatic and presymptomatic patients carrying the Swedish familial Alzheimer disease mutation
- et al.
Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid beta-protein in both transfected cells and transgenic mice
Nature Med.
(1997) - et al.
Cells with a familial Alzheimer's disease mutation produce authentic beta-peptide
Neuroreport
(1993)
Increased amyloid-beta42 (43) in brains of mice expressing mutant presenilin I
Nature
(1996)
Identification, transmembrane orientation and biogenesis of the amyloid A4 precursor of Alzheimer's disease
EMBO J.
(1988)
Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's disease
Nature
(1991)
Amyloid B peptide is produced by cultured cells during normal metabolism
Nature
(1992)
Amyloid beta protein (A beta) deposition: A beta 42 (43) precedes A beta 40 in Down syndrome
Ann. Neurol.
(1995)
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2021, Physiology and BehaviorCitation Excerpt :The pathology of AD is closely related to the accumulation of extracellular amyloid-β (Aβ) (Aβ40 and Aβ42 isoforms of Aβ). The formation of AD-associated senile plaques is mainly due to the Aβ42 isoforms [10, 45] and later intracellular neurofibrillary tangles of hyperphosphorylated tau neurofibrillary tangles, which cause synaptic dysfunction and neuronal loss [44]. However, Aβ pathological metabolism is earlier and precedes the formation of tau tangles and the AD symptoms [4, 20].
Identification of amyloid beta in small extracellular vesicles: Via Raman spectroscopy
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