PICALM and Alzheimer’s Disease: An Update and Perspectives
Open accessAbstract
Genome-wide association studies (GWAS) have identified the PICALM (Phosphatidylinositol binding clathrin-assembly protein) gene as the most significant genetic susceptibility locus after APOE and BIN1. PICALM is a clathrin-adaptor protein that plays a critical role in clathrin-mediated endocytosis and autophagy. Since the effects of genetic variants of PICALM as AD-susceptibility loci have been confirmed by independent genetic studies in several distinct cohorts, there has been a number of in vitro and in vivo studies attempting to elucidate the underlying mechanism by which PICALM modulates AD risk. While differential modulation of APP processing and Aβ transcytosis by PICALM has been reported, significant effects of PICALM modulation of tau pathology progression have also been evidenced in Alzheimer’s disease models. In this review, we summarize the current knowledge about PICALM, its physiological functions, genetic variants, post-translational modifications and relevance to AD pathogenesis.
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PICALM expression in patients with AD may also be influenced by cell type, MG state and disease stage.
“Although our study indicates a reduced PICALM expression in LOAD-risk-allele iMGs, PICALM expression in patients with AD may also be influenced by cell type, MG state and disease stage31,56.”
From PICALM Alzheimer’s risk allele causes aberrant lipid droplets in microglia (2025) · cites this paper as [31]
Section 3.3.1 says PICALM expression is dysregulated during AD progression, while section 3.4 and Discussion section 4.1 describe differing expression across cell types in AD brains. Section 3.4 also reports microglial PICALM upregulation correlated with AD pathology, but the cited paper does not establish that microglial state itself influences PICALM expression. (LLM, conf=0.82)
Experimental — accuracy not yet measuredPICALM has a role in clathrin-mediated endocytosis in non-MG cells.
“and the role of PICALM in clathrin-mediated endocytosis in non-MG cells31,32”
From PICALM Alzheimer’s risk allele causes aberrant lipid droplets in microglia (2025) · cites this paper as [31]
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Effect of Clathrin Assembly Lymphoid Myeloid Leukemia Protein Depletion on Clathrin Coat Formation
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Evidence for CALM in Directing VAMP2 Trafficking
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Self-citationEarly axonopathy preceding neurofibrillary tangles in mutant tau transgenic mice
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Self-citationTau filaments in neurodegenerative diseases
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The Role of PICALM in Alzheimer’s Disease
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Distribution and Expression of Picalm in Alzheimer Disease
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Deregulation of neuronal miRNAs induced by amyloid-β or TAU pathology
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Untangling Tau and Iron: Exploring the Interaction Between Iron and Tau in Neurodegeneration
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Variant calling on the GRCh38 assembly with the data from phase three of the 1000 Genomes Project
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Quantitative phosphoproteomic profiling of human non-small cell lung cancer tumors
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m-Calpain (calcium-activated neutral proteinase) in Alzheimer's disease brains
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Inferring protein expression changes from mRNA in Alzheimer’s dementia using deep neural networks
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PICALM Rescues Endocytic Defects Caused by the Alzheimer’s Disease Risk Factor APOE4
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Association of CLU and PICALM variants with Alzheimer's disease
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Genetics of PICALM Expression and Alzheimer's Disease
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Modulation of γ- and β-secretases as early prevention against Alzheimer's disease
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Multiple loci influencing hippocampal degeneration identified by genome scan
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Cholesterol determines the cytosolic entry and seeded aggregation of tau
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Evidence that PICALM affects age at onset of Alzheimer's dementia in Down syndrome
Jones, E. L., Mok, K., Hanney, M., Harold, D., Sims, R., Williams, J., & Ballard, C. (2013) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2013.03.018 · Cited by 47 · see citing works
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Role of the clathrin adaptor PICALM in normal hematopoiesis and polycythemia vera pathophysiology
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Picalm reduction exacerbates tau pathology in a murine tauopathy model
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Self-citationAlzheimer's disease risk genes and the age-at-onset phenotype
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Altered protein phosphorylation as a resource for potential AD biomarkers
Henriques, A. G., Müller, T., Oliveira, J. M., Cova, M. M., Silva, C. B. D. C. E., & Silva, O. A. B. D. C. E. (2016) · Scientific Reports · doi:10.1038/srep30319 · Cited by 40 · see citing works
The convergence of endosomal and autophagosomal pathways
Tian, Y., Chang, J. C., Greengard, P., & Flajolet, M. (2014) · Autophagy · doi:10.4161/auto.27802 · Cited by 39 · see citing works
Reduction of AP180 and CALM Produces Defects in Synaptic Vesicle Size and Density
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miR155 regulation of behavior, neuropathology, and cortical transcriptomics in Alzheimer's disease
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Cleavage of purified neuronal clathrin assembly protein (CALM) by caspase 3 and calpain
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Partial loss of CALM function reduces Aβ42 production and amyloid depositionin vivo
Kanatsu, K., Hori, Y., Takatori, S., Watanabe, T., Iwatsubo, T., & Tomita, T. (2016) · Human Molecular Genetics · doi:10.1093/hmg/ddw239 · Cited by 25 · see citing works
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Exosomal MicroRNA-155 Inhibits Enterovirus A71 Infection by Targeting PICALM
Wu, J., Gu, J., Shen, L., Fang, D., Zou, X., Cao, Y., Wang, S., & Mao, L. (2019) · International Journal of Biological Sciences · doi:10.7150/ijbs.36388 · Cited by 23 · see citing works
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Dysregulation of Phosphoinositide 5-Phosphatases and Phosphoinositides in Alzheimer's Disease
Ando, K., Erneux, C., Homa, M., Houben, S., de Fisenne, M.-A., Brion, J., & Leroy, K. (2021) · Frontiers in Neuroscience · doi:10.3389/fnins.2021.614855 · Cited by 18 · see citing works
Self-citationAn intronic PICALM polymorphism, rs588076, is associated with allelic expression of a PICALMisoform
Parikh, I. J., Medway, C., Younkin, S. G., Fardo, D. W., & Estus, S. (2014) · Molecular Neurodegeneration · doi:10.1186/1750-1326-9-32 · Cited by 17 · see citing works
Modulation of PICALM Levels Perturbs Cellular Cholesterol Homeostasis
Mercer, J. L., Argus, J. P., Crabtree, D. M., Keenan, M. M., Wilks, M. Q., Chi, J.-T. A., Bensinger, S. J., Lavau, C. P., & Wechsler, D. S. (2015) · PLOS ONE · doi:10.1371/journal.pone.0129776 · Cited by 17 · see citing works
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Alpha adaptins show isoform‐specific association with neurofibrillary tangles in Alzheimer's disease
Srinivasan, S., Gál, J., Bachstetter, A. D., & Nelson, P. T. (2021) · Neuropathology and Applied Neurobiology · doi:10.1111/nan.12776 · Cited by 15 · see citing works
The impact of PICALM genetic variations on reserve capacity of posterior cingulate in AD continuum
Xu, W., Wang, H.-F., Tan, L., Tan, M., Tan, C.-C., Zhu, X., Miao, D., Yu, W.-J., Jiang, T., Tan, L., et al. (2016) · Scientific Reports · doi:10.1038/srep24480 · Cited by 14 · see citing works
Xu, W., Initiative, A. D. N., Tan, C., Cao, X., & Tan, L. (2020) · Aging · doi:10.18632/aging.103814 · Cited by 14 · see citing works
Liu, Z., Dai, X., Zhang, J., Li, X., Chen, Y., Ma, C., Chen, K., Peng, D., & Zhang, Z. (2017) · Molecular Neurobiology · doi:10.1007/s12035-016-0358-5 · Cited by 12 · see citing works
Chang, Y., Huang, C., Huang, S., Hsu, S. W., Chang, W. ‐., Lee, J. ‐., & Chang, C. (2018) · Genes Brain & Behavior · doi:10.1111/gbb.12490 · Cited by 11 · see citing works
ANTH domains within CALM, HIP1R, and Sla2 recognize ubiquitin internalization signals
Pashkova, N., Gakhar, L., Yu, L., Schnicker, N. J., Minard, A. Y., Winistorfer, S., Johnson, I. E., & Piper, R. C. (2021) · eLife · doi:10.7554/elife.72583 · Cited by 11 · see citing works
PICALM regulates cathepsin D processing and lysosomal function
Hattersley, K. J., Carosi, J. M., Hein, L. K., Bensalem, J., & Sargeant, T. J. (2021) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2021.07.024 · Cited by 10 · cited 9× · see citing works
“This critical role of PICALM in autophagy is strengthened by another study showing that loss of exon 1 of PICALM in HeLa cells leads to an augmentation of lysosomal enzymes in the endosome-enriched fraction and accumulation of autophagy substrates such as APP-CTFs [48].”
BackgroundInfluentialKolay, S., & Diamond, M. I. (2020) · FEBS Open Bio · doi:10.1002/2211-5463.12928 · Cited by 8 · see citing works
Пономарева, Н. В., Андреева, Т. В., Протасова, М. А., Filippova, Y. V., Kolesnikova, E. P., Fokin, V. F., Illarioshkin, S. N., & Rogaev, E. I. (2018) · Biochemistry (Moscow) · doi:10.1134/s0006297918090092 · Cited by 6 · see citing works
Zhu, B., Li, L., Zhang, L., Yang, S., Tian, Y., Guo, S., Zhang, W., & Zhao, Z. (2018) · Metabolic Brain Disease · doi:10.1007/s11011-018-0291-6 · Cited by 2 · see citing works
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Microglia in Alzheimer’s disease: pathogenesis, mechanisms, and therapeutic potentials
Miao, J., Ma, H., Yang, Y., Liao, Y., Lin, C., Zheng, J., Yu, M., & Lan, J. (2023) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2023.1201982 · Cited by 293 · see citing works
Tijms, B. M., Vromen, E. M., Mjaavatten, O., Holstege, H. H., Reus, L. M., van der Lee, S. J., Wesenhagen, K. E. J., Lorenzini, L., Vermunt, L., Venkatraghavan, V., et al. (2024) · Nature Aging · doi:10.1038/s43587-023-00550-7 · Cited by 222 · see citing works
Zhang, Z., Yu, K., You, Y., Jiang, P., Wu, Z., Deture, M. A., Dickson, D. W., Ikezu, S., Peng, J., & Ikezu, T. (2023) · Journal of Extracellular Vesicles · doi:10.1002/jev2.12358 · Cited by 67 · see citing works
PICALM Alzheimer’s risk allele causes aberrant lipid droplets in microglia
Kozlova, A., Zhang, S., Sudwarts, A., Zhang, H., Smirnou, S., Byeon, S. K., Thapa, C., Sun, X., Stephenson, K., Zhao, X., et al. (2025) · Nature · doi:10.1038/s41586-025-09486-x · Cited by 53 · see citing works
“Although our study indicates a reduced PICALM expression in LOAD-risk-allele iMGs, PICALM expression in patients with AD may also be influenced by cell type, MG state and disease stage 31,56 .”
Arnsten, A. F. T., Tredici, K. D., Barthélemy, N. R., Gabitto, M. I., van Dyck, C. H., Lein, E. S., Braak, H., & Datta, D. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70404 · Cited by 37 · see citing works
Genetic insights into immune mechanisms of Alzheimer’s and Parkinson’s disease
Nott, A., & Holtman, I. R. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1168539 · Cited by 31 · see citing works
Whole exome sequencing analyses identified novel genes for Alzheimer's disease and related dementia
Zhang, Y.-R., Wu, B., Chen, S., Yang, L., Deng, Y., Guo, Y. X., Wu, X., Liu, W., Kang, J., Feng, J., et al. (2024) · Alzheimer s & Dementia · doi:10.1002/alz.14181 · Cited by 28 · see citing works
Diabetes, Alzheimer's Disease Risk Factors, and the Cafeteria Diet: A Comprehensive Review
Abubakar, M., Giri, A., Goel, F., Khan, M., Gupta, J., Kumar, D., Kaushik, M., Nand, S., & Kumar, N. (2025) · Current Neuropharmacology · doi:10.2174/011570159x384737250626094315 · Cited by 29 · see citing works
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Cell type-specific functions of Alzheimer's disease endocytic risk genes
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The potential of cricMAN1A2 as a novel biomarker for gout diagnosisPreprint
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PICALM :: MLLT10 translocated leukemia
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- Authors
- Ando, K., Nagaraj, S., Küçükali, F., de Fisenne, M.-A., Kosa, A.-C., Doeraene, E., Lopez Gutierrez, L., Brion, J.-P., & Leroy, K.
- Affiliations
- Laboratory of Histology, Neuropathology and Neuroanatomy, Faculty of Medicine, Université Libre de Bruxelles, ULB Neuroscience Institute, 808 Route de Lennik, 1070 Brussels, Belgium
- Université Libre de Bruxelles (BE)
- University of Antwerp (BE)
- ORCID
- Venue
- Cells
- Publisher
- MDPI AG
- Published
- 2022-12-10
- Volume
- 11
- Issue
- 24
- Pages
- 3994
- ISSN
- 2073-4409 (ISSN-L)
- PMC
- PMC9776874
- OpenAlex
- W4312125675
- Cited by
- 104
- References
- 165
- Citations by year
- 2026: 32 · 2025: 34 · 2024: 25 · 2023: 13
- FWCI
- 2.48
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cells (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Dépôt institutionnel de l'Université libre de Bruxelles (Université Libre de Bruxelles) (submittedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Belgian Fonds de la Recherche Scientifique Médicale (2019/0027, 14001, 2021/0028)
- Fund Aline (King Baudouin Foundation) (2019/0027, 14001, 2021/0028)
- Foundation for Alzheimer Research (FRA/SAO) (2019/0027, 14001, 2021/0028)
- Génicot Fund of ULB (2019/0027, 14001, 2021/0028)
- 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
- PICALM, Alzheimer's disease, genetic susceptibility, clathrin-mediated endocytosis, autophagy, clathrin adaptor proteins, APP processing, tau pathology, post-translational modification, genetic variants
- MeSH terms
- Alzheimer Disease, Clathrin, Humans, Genetic Predisposition to Disease, Monomeric Clathrin Assembly Proteins, Genome-Wide Association Study, Genetic Loci
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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