ArticleHuman molecular genetics2012
Abnormal interaction of VDAC1 with amyloid beta and phosphorylated tau causes mitochondrial dysfunction in Alzheimer's disease.
Article in Human molecular genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 203 papers, 1 of them a synthesis that pooled it.
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Who cites it
203 citing papers in PubMed, 1 synthesis or guideline pooled it, 341 citations in OpenAlex.
- Non-coding RNAs and Mitochondrial Dysfunction in Alzheimer's Disease: A Systematic Review.Molecular neurobiology · 2026Pooled it
- Role of voltage-dependent anion channel 1 in neurodegeneration: Mechanisms, implications, and therapeutic potential.Neural regeneration research · 2026Article
- Mitochondrial Voltage-Dependent Anion Channel: From a Passive Pore to a Cellular Hub Through Protein Complexation.International journal of molecular sciences · 2026Review
- Multitarget Actions of Pentacyclic Triterpenic Acids in Alzheimer's Disease: Mechanistic Insights.Molecules (Basel, Switzerland) · 2026Review
- Multi-Target-Directed Ligands (MTDLs) as Potential Therapeutic Candidates Targeting Multiple Pathogenic Factor of Alzheimer's Disease.CNS neuroscience & therapeutics · 2026Review
- The role of 2-Oxoglutarate dehydrogenase complex mitochondrial enzyme in alzheimer's disease: a literature review and bioinformatics workflow.Metabolic brain disease · 2026Review
- Peripheral Mitochondrial Energetics are Associated with Cortical Neurophysiological Alterations in Alzheimer's Disease.medRxiv : the preprint server for health sciences · 2026Article
- Amyloid-β and Mitochondrial Membranes: A Missing Link in Alzheimer's Pathogenesis.Molecular neurobiology · 2026Review
- Glycyrrhizic Acid Attenuates AβCells · 2026Article
- Signaling pathways regulating VDAC1 overexpression associated with apoptosis, pyroptosis, and ferroptosis.Cell communication and signaling : CCS · 2026Article
- p53 Interacts with VDAC1, Modulating Its Expression Level and Oligomeric State to Activate Apoptosis.Biomolecules · 2026Article
- Identification ofFrontiers in aging neuroscience · 2026Article
- Mechanisms of Alcohol Interference with Hippocampal Neurogenesis and its Repair Strategies.Molecular neurobiology · 2025Review
- Tau-Mitochondria Interactions in Neurodegeneration: Mechanisms and Therapeutic Potential.Cellular and molecular neurobiology · 2025Review
- Pathological and Functional Brain Amyloids: A New Concept Explaining the Differences.International journal of molecular sciences · 2025Review
- Temporal Interactome Mapping of Human Tau in Drosophila Reveals Progressive Mitochondrial Engagement and Porin/VDAC1-Dependent Modulation of Toxicity.International journal of molecular sciences · 2025Article
- Mitochondrial Damage and Autophagy Dysregulation in Alzheimer's Disease: Mechanisms and Therapeutic Opportunities.Neurochemical research · 2025Review
- Prefrontal cortical microglial transcriptome relates to mouse offspring executive function deficits after perinatal opioid exposure in a sex-dependent manner.Brain, behavior, and immunity · 2025Article
- Is the Voltage-Dependent Anion Channel a Major Player in Neurodegenerative Diseases?International journal of molecular sciences · 2025Review
- Intracellular accumulation of amyloid-ß is a marker of selective neuronal vulnerability in Alzheimer's disease.Nature communications · 2025Article
143 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The purpose of our study was to determine the relationship between voltage-dependent anion channel 1 protein (VDAC1) and amyloid beta (Aβ) and phosphorylated tau in Alzheimer's disease (AD). Using brain specimens from AD patients, control subjects and 6-, 12- and 24-month-old Aβ precursor protein (APP) transgenic mice, we studied VDAC1 protein levels. Further, we also studied the interaction between VDAC1 and Aβ (monomers and oligomers) and phosphorylated tau, using cortical issues from AD patients, control subjects, APP, APP/PS1 and 3XTg.AD mice. We also studied age- and VDAC1-linked, mutant APP/Aβ-induced mitochondrial dysfunction in APP and non-transgenic wild-type (WT) mice. We found progressively increased levels of VDAC1 in the cortical tissues from the brains of patients with AD, relative to control subjects, and significantly increased levels of VDAC1 in the cerebral cortices of 6-, 12- and 24-month-old APP transgenic mice, relative to the age-matched control WT mice. Interestingly, we found VDAC1 interacted with Aβ and phosphorylated tau in the brains from AD patients and from APP, APP/PS1 and 3XTg.AD mice. We found progressively increased mitochondrial dysfunction in APP mice relative to WT mice. These observations led us to conclude that VDAC1 interacts with Aβ, and phosphorylated tau may in turn block mitochondrial pores, leading to mitochondrial dysfunction in AD pathogenesis. Based on current study observations, we propose that reduced levels of VDAC1, Aβ and phosphorylated tau may reduce the abnormal interaction between VDAC1 and APP, VDAC1 and Aβ, and VDAC1 and phosphorylated tau; and that reduced levels of VDAC1, Aβ and phosphorylated tau may maintain normal mitochondrial pore opening and pore closure, ultimately leading to normal mitochondrial function, mitochondria supplying ATP to nerve terminals and boosting synaptic and cognitive function in AD.
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