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Cited by 177

The DOI matches its Crossref record; 23 of the 23 references it cites were found in a registry or an index.

Genetic dissection of Alzheimer disease, a heterogeneous disorder.

Open access
Schellenberg, G D·1995·Proceedings of the National Academy of Sciences

Abstract

The genetics of Alzheimer disease (AD) are complex and not completely understood. Mutations in the amyloid precursor protein gene (APP) can cause early-onset autosomal dominant AD. In vitro studies indicate that cells expressing mutant APPs overproduce pathogenic forms of the A beta peptide, the major component of AD amyloid. However, mutations in the APP gene are responsible for 5% or less of all early-onset familial AD. A locus on chromosome 14 is responsible for AD in other early-onset AD families and represents the most severe form of the disease in terms of age of onset and rate of decline. Attempts to identify the AD3 gene by positional cloning methods are underway. At least one additional early-onset AD locus remains to be located. In late-onset AD, the apolipoprotein E gene allele epsilon 4 is a risk factor for AD. This allele appears to act as a dose-dependent age-of-onset modifier. The epsilon 2 allele of this gene may be protective. Other late-onset susceptibility factors remain to be identified.

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Metadata

Authors
Schellenberg, G. D.
Venue
Proceedings of the National Academy of Sciences
Published
1995-09-12
Volume
92
Issue
19
Pages
8552-8559
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W2059806453
Cited by
177
References
23
FWCI
14.15
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Genetic dissection of Alzheimer disease, a heterogeneous disorder. https://app.cochat.ai/papers/10.1073/pnas.92.19.8552
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Schellenberg, G. D. (1995). Genetic dissection of Alzheimer disease, a heterogeneous disorder. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.92.19.8552

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