PICALM and Alzheimer's Disease: An Update and Perspectives

Genome-wide association studies (GWAS) have identified the (Phosphatidylinositol binding clathrin-assembly protein) gene as the most significant genetic susceptibility locus after and . PICALM is a clathrin-adaptor protein that plays a critical role in clathrin-mediated endocytosis and autophagy. Si...

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Published inCells (Basel, Switzerland) Vol. 11; no. 24; p. 3994
Main Authors Ando, Kunie, Nagaraj, Siranjeevi, Küçükali, Fahri, de Fisenne, Marie-Ange, Kosa, Andreea-Claudia, Doeraene, Emilie, Lopez Gutierrez, Lidia, Brion, Jean-Pierre, Leroy, Karelle
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 01.12.2022
MDPI
Subjects
Age
Alzheimer Disease - genetics
Alzheimer Disease - metabolism
Alzheimer's disease
Amino acids
amyloid β
Apolipoprotein E
Autophagy
Binding proteins
Biosynthesis
Bone marrow
Brain
Cholesterol
Chromosomes
Clathrin
Clathrin - metabolism
Development and progression
Endocytosis
Fibroblasts
Genes
Genetic diversity
Genetic Loci
Genetic Predisposition to Disease
Genome-wide association studies
Genome-Wide Association Study
Genomes
Genomics
GWAS
Health aspects
Health risk assessment
Homeostasis
Humans
Leukemia
microglia
Monomeric Clathrin Assembly Proteins - genetics
Monomeric Clathrin Assembly Proteins - metabolism
Mutation
Neurodegenerative diseases
neurofibrillary tangles
Neuropathology
Pathogenesis
Pathology
Peptides
Phosphatidylinositol
PICALM
Post-translation
Proteins
Review
Susceptibility
Tau protein
Belgium
GWAS
Alzheimer’s disease
amyloid β
microglia
neurofibrillary tangles
PICALM
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Abstract Genome-wide association studies (GWAS) have identified the (Phosphatidylinositol binding clathrin-assembly protein) gene as the most significant genetic susceptibility locus after and . PICALM is a clathrin-adaptor protein that plays a critical role in clathrin-mediated endocytosis and autophagy. Since the effects of genetic variants of 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.
AbstractList 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.
Genome-wide association studies (GWAS) have identified the (Phosphatidylinositol binding clathrin-assembly protein) gene as the most significant genetic susceptibility locus after and . PICALM is a clathrin-adaptor protein that plays a critical role in clathrin-mediated endocytosis and autophagy. Since the effects of genetic variants of 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.
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.
Audience Academic
Author Doeraene, Emilie
Brion, Jean-Pierre
Ando, Kunie
Lopez Gutierrez, Lidia
Leroy, Karelle
Küçükali, Fahri
de Fisenne, Marie-Ange
Kosa, Andreea-Claudia
Nagaraj, Siranjeevi
AuthorAffiliation 1 Laboratory of Histology, Neuropathology and Neuroanatomy, Faculty of Medicine, Université Libre de Bruxelles, ULB Neuroscience Institute, 808 Route de Lennik, 1070 Brussels, Belgium
2 Complex Genetics of Alzheimer’s Disease Group, VIB Center for Molecular Neurology, VIB Antwerp, Department of Biomedical Sciences, University of Antwerp, 2000 Antwerp, Belgium
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  surname: Leroy
  fullname: Leroy, Karelle
  organization: Laboratory of Histology, Neuropathology and Neuroanatomy, Faculty of Medicine, Université Libre de Bruxelles, ULB Neuroscience Institute, 808 Route de Lennik, 1070 Brussels, Belgium
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Keywords GWAS
Alzheimer’s disease
amyloid β
microglia
neurofibrillary tangles
PICALM
Language English
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– name: Basel
PublicationTitle Cells (Basel, Switzerland)
PublicationTitleAlternate Cells
PublicationYear 2022
Publisher MDPI AG
MDPI
Publisher_xml – name: MDPI AG
– name: MDPI
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Snippet Genome-wide association studies (GWAS) have identified the (Phosphatidylinositol binding clathrin-assembly protein) gene as the most significant genetic...
Genome-wide association studies (GWAS) have identified the PICALM (Phosphatidylinositol binding clathrin-assembly protein) gene as the most significant genetic...
Genome-wide association studies (GWAS) have identified the PICALM (Phosphatidylinositol binding clathrin-assembly protein) gene as the most significant genetic...
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StartPage 3994
SubjectTerms Age
Alzheimer Disease - genetics
Alzheimer Disease - metabolism
Alzheimer's disease
Amino acids
amyloid β
Apolipoprotein E
Autophagy
Binding proteins
Biosynthesis
Bone marrow
Brain
Cholesterol
Chromosomes
Clathrin
Clathrin - metabolism
Development and progression
Endocytosis
Fibroblasts
Genes
Genetic diversity
Genetic Loci
Genetic Predisposition to Disease
Genome-wide association studies
Genome-Wide Association Study
Genomes
Genomics
GWAS
Health aspects
Health risk assessment
Homeostasis
Humans
Leukemia
microglia
Monomeric Clathrin Assembly Proteins - genetics
Monomeric Clathrin Assembly Proteins - metabolism
Mutation
Neurodegenerative diseases
neurofibrillary tangles
Neuropathology
Pathogenesis
Pathology
Peptides
Phosphatidylinositol
PICALM
Post-translation
Proteins
Review
Susceptibility
Tau protein
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Title PICALM and Alzheimer's Disease: An Update and Perspectives
URI https://www.ncbi.nlm.nih.gov/pubmed/36552756
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Volume 11
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