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Cited by 61Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

The role of CD2AP in the Pathogenesis of Alzheimer's Disease

Open access
Tao, Qing-Qing, Chen, Yu-Chao, Wu, Zhi-Ying·2019·Aging and disease
DOI 10.14336/ad.2018.1025PMC PMC6675523
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Abstract

Alzheimer’s disease (AD) is the most common neurodegenerative disease characterized by irreversible decline in cognition with unclear pathogenesis. Recently, accumulating evidence has revealed that CD2 associated protein (CD2AP), a scaffolding molecule regulates signal transduction and cytoskeletal molecules, is implicated in AD pathogenesis. Several single nucleotide polymorphisms (SNPs) in CD2AP gene are associated with higher risk for AD and mRNA levels of CD2AP are decreased in peripheral lymphocytes of sporadic AD patients. Furthermore, CD2AP loss of function is linked to enhanced Aβ production, Tau-induced neurotoxicity, abnormal neurite structure modulation and reduced blood-brain barrier integrity. This review is to summarize the recent discoveries about the genetics and known functions of CD2AP. The recent evidence concerning the roles of CD2AP in the AD pathogenesis is summarized and CD2AP can be a promising therapeutic target for AD.

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  • Cd2ap has been previously associated with Alzheimer's disease pathology aggravated by increased deposition of Aβ and Tau-induced neurotoxicity.

    “In fact, the long-term infection was also associated with low expression of Cd2ap which has been previously associated with AD pathology aggravated by increased deposition of Aβ and Tau-induced neurotoxicity87.”

    From Chlamydia pneumoniae can infect the central nervous system via the olfactory and trigeminal nerves and contributes to Alzheimer’s disease risk (2022) · cites this paper as [87]

    The Conclusions (page unavailable) link CD2AP loss of function to altered Aβ metabolism and Tau-induced neurotoxicity. The amyloidogenesis section discusses Aβ generation and levels, but does not establish that CD2AP loss increases Aβ deposition specifically. (LLM, conf=0.86)

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Cited by

Sorted by citations

Authors
Tao, Q.-Q., Chen, Y.-C., & Wu, Z.-Y.
Affiliations
Second Affiliated Hospital of Zhejiang University (CN)
Corresponding author
Wu, Zhi-Ying
ORCID
Venue
Aging and disease
Publisher
Aging and Disease
Published
2019
Volume
10
Issue
4
Pages
901
ISSN
2152-5250 (ISSN-L)
DOI
10.14336/ad.2018.1025
PMC
PMC6675523
OpenAlex
W2904830263
Cited by
61
References
13
Citations by year
2026: 3 · 2025: 15 · 2024: 13 · 2023: 10 · 2022: 7 · 2021: 5 · 2020: 7 · 2019: 1
FWCI
0.43
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Aging and Disease (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
National Natural Science Foundation of China (81600922)
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
CD2AP, Alzheimer's disease pathogenesis, single nucleotide polymorphisms, amyloid-beta production, blood-brain barrier integrity, peripheral blood lymphocytes, therapeutic target, scaffold proteins

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