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Table representation of search results timeline featuring number of search results per year.

Year Number of Results
1988 1
1990 19
1991 61
1992 20
1993 22
1994 25
1995 31
1996 40
1997 25
1998 45
1999 47
2000 52
2001 64
2002 83
2003 64
2004 104
2005 111
2006 101
2007 112
2008 137
2009 185
2010 205
2011 166
2012 175
2013 171
2014 153
2015 166
2016 171
2017 192
2018 210
2019 79
2020 1
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2,743 results
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Page 1
The case for rejecting the amyloid cascade hypothesis.
Herrup K. Nat Neurosci 2015 - Review. PMID 26007212
Nearly 20 years ago, with the combination of observations from biochemistry, neuropathology and genetics, a compelling hypothesis known as the amyloid cascade hypothesis was formulated. ...This Perspective explores the proposition that we are over-reliant on amyloid to define and diagnose AD and that the time has come to face our fears and reject the amyloid cascade hypothesis....
Nearly 20 years ago, with the combination of observations from biochemistry, neuropathology and genetics, a compelling hypothesis kno …
Neuropathology and biochemistry of Aβ and its aggregates in Alzheimer's disease
Thal DR, et al. Acta Neuropathol 2015 - Review. PMID 25534025
Alzheimer's disease (AD) is characterized by β-amyloid plaques and intraneuronal τ aggregation usually associated with cerebral amyloid angiopathy (CAA). ...Different variants of Aβ peptides may result from alternative processing or from mutations that lead to rare forms of familial AD. ...
Alzheimer's disease (AD) is characterized by β-amyloid plaques and intraneuronal τ aggregation usually associated with cerebral am
Genetic Risk Factors for Alzheimer Disease: Emerging Roles of Microglia in Disease Pathomechanisms
Takatori S, et al. Adv Exp Med Biol 2019 - Review. PMID 30747419
The accumulation of aggregated amyloid β (Aβ) peptides in the brain is deeply involved in Alzheimer disease (AD) pathogenesis. ...
The accumulation of aggregated amyloid β (Aβ) peptides in the brain is deeply involved in Alzheimer disease (AD) pathogenesis. …
Prion and Prion-Like Protein Strains: Deciphering the Molecular Basis of Heterogeneity in Neurodegeneration
Scialò C, et al. Viruses 2019 - Review. PMID 30875755 Free PMC article.
Despite a lack of infectivity, experimental data show that the replication and propagation of neurodegenerative disease-related proteins including amyloid-β (Aβ), tau, α-synuclein and the transactive response DNA-binding protein of 43 kDa (TDP-43) share a similar pathological mechanism with prions. ...
Despite a lack of infectivity, experimental data show that the replication and propagation of neurodegenerative disease-related proteins inc …
Cognitive and emotional alterations in App knock-in mouse models of Aβ amyloidosis
Sakakibara Y, et al. BMC Neurosci 2018. PMID 30055565 Free PMC article.
BACKGROUND: Alzheimer's disease (AD), the most common cause of dementia, is characterized by the progressive deposition of amyloid-β (Aβ) peptides and neurofibrillary tangles. Mouse models of Aβ amyloidosis generated by knock-in (KI) of a humanized Aβ sequence provide distinct advantages over traditional transgenic models that rely on overexpression of amyloid precursor protein (APP). ...
BACKGROUND: Alzheimer's disease (AD), the most common cause of dementia, is characterized by the progressive deposition of amyloid-β …
A genetic cause of Alzheimer disease: mechanistic insights from Down syndrome
Wiseman FK, et al. Nat Rev Neurosci 2015 - Review. PMID 26243569 Free PMC article.
It is thought that this risk is conferred by the presence of three copies of the gene encoding amyloid precursor protein (APP)--an Alzheimer disease risk factor--although the possession of extra copies of other chromosome 21 genes may also play a part. ...
It is thought that this risk is conferred by the presence of three copies of the gene encoding amyloid precursor protein (APP)--an Al …
New Mechanism of Amyloid Fibril Formation.
Galzitskaya O. Curr Protein Pept Sci 2019 - Review. PMID 30686252
Polymorphism is a specific feature of the amyloid structures. We have studied the amyloid structures and the process of their formation using the synthetic and recombinant preparations of Aβ peptides and their three fragments. ...Identification of regions in the protein chains that form the backbone of amyloid fibril is a direction in the investigation of amyloid formation. ...
Polymorphism is a specific feature of the amyloid structures. We have studied the amyloid structures and the process of their …
Paradoxical effects of mutant ubiquitin on Aβ plaque formation in an Alzheimer mouse model
Verheijen BM, et al. Neurobiol Aging 2018. PMID 30216939 Free article.
Amyloid-β (Aβ) plaques are a prominent pathological hallmark of Alzheimer's disease (AD). They consist of aggregated Aβ peptides, which are generated through sequential proteolytic processing of the transmembrane protein amyloid precursor protein (APP) and several Aβ-associated factors. ...
Amyloid-β (Aβ) plaques are a prominent pathological hallmark of Alzheimer's disease (AD). They consist of aggregated Aβ peptides
Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's disease.
Goate A, et al. Nature 1991. PMID 1671712
A locus segregating with familial Alzheimer's disease (AD) has been mapped to chromosome 21, close to the amyloid precursor protein (APP) gene. ...This mutation causes an amino-acid substitution (Val----Ile) close to the carboxy terminus of the beta-amyloid peptide. Screening other cases of familial AD revealed a second unrelated family in which this variant occurs. ...
A locus segregating with familial Alzheimer's disease (AD) has been mapped to chromosome 21, close to the amyloid precursor protein ( …
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