ArticleThe Journal of biological chemistry2019
CD2-associated protein (CD2AP) overexpression accelerates amyloid precursor protein (APP) transfer from early endosomes to the lysosomal degradation pathway.
Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 52 citations in OpenAlex.
- Endosome traffic in rheumatic diseases: mechanistic insights and therapeutic opportunities.Nature reviews. Rheumatology · 2026Review
- Article
- CD2AP at the junction of nephropathy and Alzheimer's disease.Molecular neurodegeneration · 2025Review
- Biomarker identification for Alzheimer's disease through integration of comprehensive Mendelian randomization and proteomics data.Journal of translational medicine · 2025Article
- APP lysine 612 lactylation ameliorates amyloid pathology and memory decline in Alzheimer's disease.The Journal of clinical investigation · 2025Article
- Identification of a ubiquitin-binding domain protein, CD2AP, in predicting the prognosis and treatment of lung adenocarcinoma.Frontiers in immunology · 2025Article
- CD2AP deficiency aggravates Alzheimer's disease phenotypes and pathology through p38 MAPK activation.Translational neurodegeneration · 2024Article
- Microglial CD2AP deficiency exerts protection in an Alzheimer's disease model of amyloidosis.Molecular neurodegeneration · 2024Article
- The Alzheimer's Disease Risk Gene CD2AP Functions in Dendritic Spines by Remodeling F-Actin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Decoding the Cellular Trafficking of Prion-like Proteins in Neurodegenerative Diseases.Neuroscience bulletin · 2024Review
- Regulation of the hippocampal translatome by Apoer2-ICD release.Molecular neurodegeneration · 2023Article
- Endolysosomal impairment by binding of amyloid beta or MAPT/Tau to V-ATPase and rescue via the HYAL-CD44 axis in Alzheimer disease.Autophagy · 2023Article
- The Cleavage-Specific Tau 12A12mAb Exerts an Anti-Amyloidogenic Action by Modulating the Endocytic and Bioenergetic Pathways in Alzheimer's Disease Mouse Model.International journal of molecular sciences · 2023Article
- Moving beyond amyloid and tau to capture the biological heterogeneity of Alzheimer's disease.Trends in neurosciences · 2023Review
- Endosomal trafficking and related genetic underpinnings as a hub in Alzheimer's disease.Journal of cellular physiology · 2022Review
- Association of CD2AP neuronal deposits with Braak neurofibrillary stage in Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2022Article
- The role of Alzheimer's disease risk genes in endolysosomal pathways.Neurobiology of disease · 2022Review
- Neuronal ROS-induced glial lipid droplet formation is altered by loss of Alzheimer's disease-associated genes.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Multi-tissue neocortical transcriptome-wide association study implicates 8 genes across 6 genomic loci in Alzheimer's disease.Genome medicine · 2021Article
- Dieckol Ameliorates Aβ Production via PI3K/Akt/GSK-3β Regulated APP Processing in SweAPP N2a Cell.Marine drugs · 2021Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A hallmark of Alzheimer's disease (AD) pathology is the appearance of senile plaques, which are composed of β-amyloid (Aβ) peptides. Aβ is produced by sequential cleavages of amyloid precursor protein (APP) by β- and γ-secretases. These cleavages take place in endosomes during intracellular trafficking of APP through the endocytic and recycling pathways. Genome-wide association studies have identified several risk factors for late-onset AD, one of which is CD2-associated protein (CD2AP), an adaptor molecule that regulates membrane trafficking. Although CD2AP's involvement in APP trafficking has recently been reported, how APP trafficking is regulated remains unclear. We sought to address this question by investigating the effect of CD2AP overexpression or knockdown on the intracellular APP distribution and degradation of APP in cultured COS-7 and HEK293 cells. We found that overexpression of CD2AP increases the localization of APP to Rab7-positive late endosomes, and decreases its localization to Rab5-positive early endosomes. CD2AP overexpression accelerated the onset of APP degradation without affecting its degradation rate. Furthermore, nutrient starvation increased the localization of APP to Rab7-positive late endosomes, and CD2AP overexpression stimulated starvation-induced lysosomal APP degradation. Moreover, the effect of CD2AP on the degradation of APP was confirmed by CD2AP overexpression and knockdown in primary cortical neurons from mice. We conclude that CD2AP accelerates the transfer of APP from early to late endosomes. This transfer in localization stimulates APP degradation by reducing the amount of time before degradation initiation. Taken together, these results may explain why impaired CD2AP function is a risk factor for AD.
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