Cited by 406Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

ALZHEIMER'S DISEASE: Genetic Studies and Transgenic Models

Price, Donald L., Tanzi, Rudolph E., Borchelt, David R., Sisodia, Sangram S.·1998·Annual Review of Genetics

Abstract

Recent advances in a variety of areas of research, particularly in genetics and in transgenic (Tg)/gene targeting approaches, have had a substantial impact on our understanding of Alzheimer's disease (AD) and related disorders. After briefly reviewing the progress that has been made in diagnostic assessments of patients with senile dementia and in investigations of the neuropathology of AD, we discuss some of the genes/proteins that are causative or risk factors for this disease, including those encoding amyloid precursor protein, presenilin 1 and 2, and apolipoprotein E. In addition, we comment on several potential new candidate loci/genes. Subsequently, we review selected recent reports of analyses of a variety of lines of Tg mice that show several neuropathological features of AD, including A beta-amyloid deposits and dystrophic neurites. Finally, we discuss the several important issues in future investigations of Tg mice, with particular emphasis on the influences of genetic strains on phenotype, especially behavior, and strategies for making new models of neurodegenerative disorders. We believe that investigations of these Tg models will (a) enhance understanding of the relationships between impaired performance on memory tasks and the pathological/biochemical abnormalities in brain, (b) help to clarify pathogenic mechanisms in vivo, (c) lead to identification of new therapeutic targets, and (d) allow testing of new treatment strategies first in mice and then, if success…

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Crossref · 10.1146/annurev.genet.32.1.461

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  • Aβ42 plays a pivotal role in Alzheimer's disease pathogenesis.

    “Numerous studies have established a pivotal role for A␤42 in Alzheimer's disease (AD) pathogenesis.”

    From Aβ40 Inhibits Amyloid Deposition<i>In Vivo</i> (2007) · cites this paper as Price et al., 1998

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Authors
Price, D. L., Tanzi, R. E., Borchelt, D. R., & Sisodia, S. S.
Affiliations
Johns Hopkins University (US)
Venue
Annual Review of Genetics
Published
1998-12
Volume
32
Issue
1
Pages
461-493
ISSN
  • 0066-4197 (ISSN-L)
  • 1545-2948
OpenAlex
W2122230892
Cited by
406
References
21
Citations by year
2025: 6 · 2024: 3 · 2023: 7 · 2022: 5 · 2021: 7 · 2020: 8 · 2019: 5 · 2018: 10 · 2017: 10 · 2016: 12 · 2015: 6 · 2014: 10 · 2013: 11 · 2012: 15
FWCI
4.20
Type
journal article
Language
en
Open access
closed
Locations
  • Annual Review of Genetics (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institute on Aging (R01AG008325, AG08325, P50AG005146, AG 05146)
  • National Institute of Mental Health
  • National Institute of Neurological Disorders and Stroke (NS-20471)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
Alzheimer's disease, transgenic mouse model, genetic risk factors, amyloid precursor protein, presenilin 1, presenilin 2, apolipoprotein E, neuropathology, amyloid-beta deposition, dystrophic neurites, candidate genes, memory impairment, neurodegenerative disease models, therapeutic target
MeSH terms
Alzheimer Disease, Animals, Apolipoproteins E, Disease Models, Animal, Humans, Membrane Proteins, Mice, Transgenic, Mutation, Phenotype, Amyloid beta-Protein Precursor, Caenorhabditis elegans, Mice, Knockout, Mice, Presenilin-1, Presenilin-2

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