ArticleJournal of neuropathology and experimental neurology2016
Subcellular Changes in Bridging Integrator 1 Protein Expression in the Cerebral Cortex During the Progression of Alzheimer Disease Pathology.
Article in Journal of neuropathology and experimental neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 43 citations in OpenAlex.
- Bridging autophagy and endolysosomal dysfunction: Role of bridging integrator 1 in Alzheimer's disease.Neural regeneration research · 2026Article
- BIN1 gain-of-function in the presynaptic compartment leads to isoform-specific synaptotoxicity.Alzheimer's research & therapy · 2026Article
- Interactome mapping in human excitatory neurons reveals novel risk genes and pathways in Alzheimer's disease.bioRxiv : the preprint server for biology · 2026Article
- Human stem cell transplantation models of Alzheimer's disease.Frontiers in aging neuroscience · 2024Review
- Loss of forebrain BIN1 attenuates hippocampal pathology and neuroinflammation in a tauopathy model.Brain : a journal of neurology · 2023Article
- BIN1 is a key regulator of proinflammatory and neurodegeneration-related activation in microglia.Molecular neurodegeneration · 2022Article
- The Alzheimer susceptibility gene BIN1 induces isoform-dependent neurotoxicity through early endosome defects.Acta neuropathologica communications · 2022Article
- Lack of association between bridging integrator 1 (Alzheimer's & dementia (New York, N. Y.) · 2022Article
- The Mechanistic Role of Bridging Integrator 1 (BIN1) in Alzheimer's Disease.Cellular and molecular neurobiology · 2021Review
- Association between methylation of BIN1 promoter in peripheral blood and preclinical Alzheimer's disease.Translational psychiatry · 2021Article
- A novel role for the late-onset Alzheimer's disease (LOAD)-associated protein Bin1 in regulating postsynaptic trafficking and glutamatergic signaling.Molecular psychiatry · 2020Article
- BIN1 protein isoforms are differentially expressed in astrocytes, neurons, and microglia: neuronal and astrocyte BIN1 are implicated in tau pathology.Molecular neurodegeneration · 2020Article
- The Expression of Activin Receptor-Like Kinase 1 (ACVRL1/ALK1) in Hippocampal Arterioles Declines During Progression of Alzheimer's Disease.Cerebral cortex communications · 2020Article
- Aberrant accrual of BIN1 near Alzheimer's disease amyloid deposits in transgenic models.Brain pathology (Zurich, Switzerland) · 2019Article
- BIN1 favors the spreading of Tau via extracellular vesicles.Scientific reports · 2019Article
- Endo-lysosomal dysregulations and late-onset Alzheimer's disease: impact of genetic risk factors.Molecular neurodegeneration · 2019Review
- Reduction of the expression of the late-onset Alzheimer's disease (AD) risk-factorThe Journal of biological chemistry · 2019Article
- Article
- Immunohistochemical Analysis of Activin Receptor-Like Kinase 1 (ACVRL1/ALK1) Expression in the Rat and Human Hippocampus: Decline in CA3 During Progression of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2018Article
- Article
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
Genome-wide association studies have established BIN1 (Bridging Integrator 1) as the most significant late-onset Alzheimer disease (AD) susceptibility locus after APOE We analyzed BIN1 protein expression using automated immunohistochemistry on the hippocampal CA1 region in 19 patients with either no, mild, or moderate-to-marked AD pathology, who had been assessed by Clinical Dementia Rating and CERAD scores. We also examined the amygdala, prefrontal, temporal, and occipital regions in a subset of these patients. In non-demented controls without AD pathology, BIN1 protein was expressed in white matter, glia, particularly oligodendrocytes, and in the neuropil in which the BIN1 signal decorated axons. With increasing severity of AD, BIN1 in the CA1 region showed: 1) sustained expression in glial cells, 2) decreased areas of neuropil expression, and 3) increased cytoplasmic neuronal expression that did not correlate with neurofibrillary tangle load. In patients with AD, both the prefrontal cortex and CA1 showed a decrease in BIN1-immunoreactive (BIN1-ir) neuropil areas and increases in numbers of BIN1-ir neurons. The numbers of CA1 BIN1-ir pyramidal neurons correlated with hippocampal CERAD neuritic plaque scores; BIN1 neuropil signal was absent in neuritic plaques. Our data provide novel insight into the relationship between BIN1 protein expression and the progression of AD-associated pathology and its diagnostic hallmarks.
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