ArticlePloS one2013
BIN1 is decreased in sporadic but not familial Alzheimer's disease or in aging.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.
- Pooled it
- Bridging autophagy and endolysosomal dysfunction: Role of bridging integrator 1 in Alzheimer's disease.Neural regeneration research · 2026Article
- Article
- Bend it like BIN1: how a membrane-curving adaptor protein shapes cardiac physiology.American journal of physiology. Heart and circulatory physiology · 2025Review
- BIN1 deficiency enhances ULK3-dependent autophagic flux and reduces dendritic size in mouse hippocampal neurons.Autophagy · 2025Article
- The Alzheimer's disease risk gene BIN1 regulates activity-dependent gene expression in human-induced glutamatergic neurons.Molecular psychiatry · 2024Article
- Cell type-specific functions of Alzheimer's disease endocytic risk genes.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024Review
- BIN1Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- BIN1 in the Pursuit of Ousting the Alzheimer's Reign: Impact on Amyloid and Tau Neuropathology.Neurotoxicity research · 2023Review
- 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
- Loss of forebrain BIN1 attenuates hippocampal pathology and neuroinflammation in a tauopathy model.Brain : a journal of neurology · 2023Article
- Altered DNA methylome profiles of blood leukocytes in Chinese patients with mild cognitive impairment and Alzheimer's disease.Frontiers in genetics · 2023Article
- Upregulation of endocytic protein expression in the Alzheimer's disease male human brain.Aging brain · 2023Article
- Genetic polymorphism in BIN1 rather than APOE is associated with poor recognition memory among men without dementia.Scientific reports · 2022Article
- The relationship of early- and late-onset Alzheimer's disease genes with COVID-19.Journal of neural transmission (Vienna, Austria : 1996) · 2022Review
- The neuronal-specific isoform of BIN1 regulates β-secretase cleavage of APP and Aβ generation in a RIN3-dependent manner.Scientific reports · 2022Article
- Evaluation of mild cognitive impairment genetic susceptibility risks in a Chinese population.BMC psychiatry · 2022Article
- The Alzheimer susceptibility gene BIN1 induces isoform-dependent neurotoxicity through early endosome defects.Acta neuropathologica communications · 2022Article
- The Mechanistic Role of Bridging Integrator 1 (BIN1) in Alzheimer's Disease.Cellular and molecular neurobiology · 2021Review
- Alzheimer's disease BIN1 coding variants increase intracellular Aβ levels by interfering with BACE1 recycling.The Journal of biological chemistry · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Bridging integrator 1 (BIN1) has been implicated in sporadic Alzheimer's disease (AD) by a number of genome wide association studies (GWAS) in a variety of populations. Here we measured BIN1 in frontal cortex samples from 24 sporadic AD and 24 age-matched non-dementia brains and correlated the expression of this protein with markers of AD. BIN1 was reduced by 87% (p=0.007) in sporadic AD compared to non-dementia controls, but BIN1 in sporadic AD did not correlate with soluble Aβ (r(s)=-0.084, p=0.698), insoluble Aβ (r(s)=0.237, p=0.269), Aβ plaque load (r(s)=0.063, p=0.771) or phospho-tau load (r(s)=-0.160, p=0.489). In contrast to our findings in sporadic AD, BIN1 was unchanged in the hippocampus from 6 cases of familial AD compared to 6 age-matched controls (p=0.488). BIN1 declined with age in a cohort of non-dementia control cases between 25 and 88 years but the correlation was not significant (rs=-0.449, p=0.081). Although BIN1 is known to have a role in endocytosis, and the processing of the amyloid precursor protein (APP) to form amyloid-β (Aβ) peptides is dependent on endocytosis, knockdown of BIN1 by targeted siRNA or the overexpression of BIN1 in a human neuroblastoma cell line (SH-SY5Y) had no effect on APP processing. These data suggest that the alteration in BIN1 is involved in the pathogenesis of sporadic, but not familial AD and is not a consequence of AD neurodegeneration or the ageing process, a finding in keeping with the numerous GWAS that implicate BIN1 in sporadic AD. However, the mechanism of its contribution remains to be established.
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Registered trials
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