The DOI matches its Crossref record; 131 of the 133 references it cites were found in a registry or an index.
Amyloid beta-induced glycogen synthase kinase 3β phosphorylated VDAC1 in Alzheimer's disease: Implications for synaptic dysfunction and neuronal damage
Open accessAbstract
Glycogen synthase kinase 3 (GSK3) is a serine/threonine protein kinase that is involved in the multiple signaling processes of a cell. Increasing evidence suggests that GSK3β plays a key role in multiple cellular processes in the progression of diabetes, obesity, Alzheimer's disease (AD), Parkinson's disease (PD), inflammatory diseases, schizophrenia, bipolar and several mood disorders, and mitochondrial diseases. Recent research has found that increased GSK3β activity is linked to the pathogenesis of AD through amyloid beta (Aβ), phosphorylated tau and mitochondrial dysfunction. Recent research has also revealed that GSK3β is elevated in AD-affected tissues and is critically involved in dissociating the voltage-dependent anion channel 1 (VDAC1) protein from hexokinases, and causing disrupted glucose metabolism, mitochondrial dysfunction and activating apoptotic cell death. The purpose of this article is to review recent research that is elucidating the role of GSK3β in AD pathogenesis. We discuss the involvement of GSK3β in the phosphorylation of VDAC1 and dissociation of VADC1 with hexokinases in AD neurons.
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“GSK3β is already known to be involved in the regulation of APP metabolism, Tau phosphorylation and synaptic functions41–43, making it a potential link between PLCγ2 and the different phenotypes associated with its downregulation.”
From PLCG2 downregulation impairs synaptic function and increases Alzheimer’s disease hallmarks in neuronal cultures (2026) · cites this paper as [41]
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Metadata
- Authors
- Reddy, P. H.
- Affiliations
- Oregon National Primate Research Center (US)
- Corresponding author
- Reddy, P. Hemachandra
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
- Publisher
- Elsevier BV
- Published
- 2013-12
- Volume
- 1832
- Issue
- 12
- Pages
- 1913-1921
- ISSN
- 0925-4439 (ISSN-L)
- PMC
- PMC3825775
- OpenAlex
- W2077701948
- Cited by
- 147
- References
- 133
- Citations by year
- 2026: 9 · 2025: 13 · 2024: 12 · 2023: 12 · 2022: 16 · 2021: 15 · 2020: 10 · 2019: 12 · 2018: 13 · 2017: 9 · 2016: 5 · 2015: 11 · 2014: 10
- FWCI
- 0.96
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NIH (AG028072, AG042178, RR000163)
- Medical Research Foundation of Oregon
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- Alzheimer's disease, glycogen synthase kinase-3β, VDAC1, amyloid-beta, hexokinase, mitochondrial dysfunction, glucose metabolism, synaptic dysfunction, neuronal injury, apoptosis
- MeSH terms
- Glycogen Synthase Kinase 3 beta, Alzheimer Disease, Animals, Humans, Neurons, Phosphorylation, Synapses, Amyloid beta-Peptides, Glycogen Synthase Kinase 3, Voltage-Dependent Anion Channel 1
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