ArticleAging and disease2021
Extracellular GAPDH Promotes Alzheimer Disease Progression by Enhancing Amyloid-β Aggregation and Cytotoxicity.
Article in Aging and disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- Multi-platform integration of brain and CSF proteomes reveals biomarker panels for Alzheimer's disease.Briefings in bioinformatics · 2026Article
- VDAC1-interacting proteins: binding site mapping and their derived peptides induce apoptosis and multifaceted cellular effects.Apoptosis : an international journal on programmed cell death · 2025Article
- Amyloid-β disrupts APP-regulated protein aggregation and dissociation from recycling endosomal membranes.The EMBO journal · 2025Article
- GraphkmerDTA: integrating local sequence patterns and topological information for drug-target binding affinity prediction and applications in multi-target anti-Alzheimer's drug discovery.Molecular diversity · 2025Article
- Biomarker Identification for Alzheimer's Disease Using a Multi-Filter Gene Selection Approach.International journal of molecular sciences · 2025Article
- Exploring glycolytic enzymes in disease: potential biomarkers and therapeutic targets in neurodegeneration, cancer and parasitic infections.Open biology · 2025Review
- Stratifying risk of Alzheimer's disease in healthy middle-aged individuals with machine learning.Brain communications · 2025Article
- "Proteinjury": a universal pathological mechanism mediated by cerebrospinal fluid in neurodegeneration and trauma.Frontiers in cell and developmental biology · 2025Review
- Dehydroamino acids and their crosslinks in Alzheimer's disease aggregates.Brain communications · 2025Article
- Unveiling biomarker detection in Alzheimer's disease: a computational approach to microarray analysis.3 Biotech · 2024Article
- Novel Insights Into DLAT's Role in Alzheimer's Disease-Related Copper Toxicity Through Microglial Exosome Dynamics.CNS neuroscience & therapeutics · 2024Article
- Systematic Analysis of Biological Processes Reveals Gene Co-expression Modules Driving Pathway Dysregulation in Alzheimer's Disease.Aging and disease · 2024Article
- Systematic Analysis of Biological Processes Reveals Gene Co-expression Modules Driving Pathway Dysregulation in Alzheimer's Disease.bioRxiv : the preprint server for biology · 2024Article
- Systems pharmacology and multi-scale mechanism of Enicostema axillare bioactives in treating Alzheimer disease.Inflammopharmacology · 2024Article
- Article
- Exploring the Role of Glycolytic Enzymes PFKFB3 and GAPDH in the Modulation of Aβ and Neurodegeneration and Their Potential of Therapeutic Targets in Alzheimer's Disease.Applied biochemistry and biotechnology · 2023Review
- Predictors of Cognitive Decline in Healthy Middle-Aged Individuals with Asymptomatic Alzheimer's Disease.Research square · 2023Article
- Protein Interactome of Amyloid-β as a Therapeutic Target.Pharmaceuticals (Basel, Switzerland) · 2023Review
- The role of sperm-specific glyceraldehyde-3-phosphate dehydrogenase in the development of pathologies-from asthenozoospermia to carcinogenesis.Frontiers in molecular biosciences · 2023Review
- Identification and validation of biomarkers based on cellular senescence in mild cognitive impairment.Frontiers in aging neuroscience · 2023Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuronal cell death at late stages of Alzheimer's disease (AD) causes the release of cytosolic proteins. One of the most abundant such proteins, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), forms stable aggregates with extracellular amyloid-β (Aβ). We detect these aggregates in cerebrospinal fluid (CSF) from AD patients at levels directly proportional to the progressive stages of AD. We found that GAPDH forms a covalent bond with Q15 of Aβ that is mediated by transglutaminase (tTG). The Q15A substitution weakens the interaction between Aβ and GAPDH and reduces Aβ-GAPDH cytotoxicity. Lentivirus-driven GAPDH overexpression in two AD animal models increased the level of apoptosis of hippocampal cells, neural degeneration, and cognitive dysfunction. In contrast,
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.