ArticleMolecular neurobiology2023
Activation of Pgk1 Results in Reduced Protein Aggregation in Diverse Neurodegenerative Conditions.
Article in Molecular neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 22 citations in OpenAlex.
- Beta 2-adrenergic pathway combats Alzheimer's disease: Restoring cognition and synaptic integrity.Neural regeneration research · 2026Article
- Dissecting Alzheimer's proteomic landscape through NULISA profiling of brain cell-specific extracellular vesicles.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Glycolysis-enhancing αAlzheimer's research & therapy · 2026Article
- Terazosin Attenuates Neuronal Pyroptosis by Regulating the Mitochondrial ROS/NLRP3 Inflammasome Axis Through Mitophagy in Cerebral Ischemia-Reperfusion Injury.The Kaohsiung journal of medical sciences · 2026Article
- A novel PGK1 activator improves Alzheimer's disease by regulating glycolysis.Alzheimer's research & therapy · 2026Article
- Spatiotemporal transcriptomic profiling reveals upregulation of glycolysis pathway genes before overt tauopathy in the PS19 mouse model.Experimental & molecular medicine · 2026Article
- The role of energy deficit in autophagy failure in Parkinson's disease.Frontiers in aging neuroscience · 2026Review
- Article
- Pgk1 activation restores endothelial metabolic homeostasis to alleviate vascular aging and atherosclerosis.Cardiovascular diabetology · 2025Article
- αPharmaceuticals (Basel, Switzerland) · 2025Review
- Dysregulated Expression of Canonical and Non-Canonical Glycolytic Enzyme Isoforms in Peripheral Blood from Subjects with Alcohol Use Disorder and from Individuals with Acute Alcohol Consumption.Antioxidants (Basel, Switzerland) · 2025Article
- Phosphoglycerate kinase 1 contributes to diabetic kidney disease through enzyme-dependent and independent manners.Cell reports. Medicine · 2025Article
- Modulation of neuronal α1-adrenergic receptor reduces tauopathy and neuroinflammation by inhibiting the STING/NF-κB/NLRP3 signaling pathway in Alzheimer's disease mice.Journal of neuroinflammation · 2025Article
- Dysregulated microRNAs in blood correlate with central nervous system neuropathology of prion disease.Veterinary research · 2025Article
- Spatiotemporal deciphering of dynamic the FUS interactome during liquid-liquid phase separation in living cells.Nature communications · 2025Article
- Deciphering the Role of Adrenergic Receptors in Alzheimer's Disease: Paving the Way for Innovative Therapies.Biomolecules · 2025Review
- Effect of low-dose terazosin on arterial stiffness improvement: A pilot study.Journal of cellular and molecular medicine · 2024Article
- A model for stimulation of enzyme activity by a competitive inhibitor based on the interaction of terazosin and phosphoglycerate kinase 1.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Bioinformatic analysis of hippocampal histopathology in Alzheimer's disease and the therapeutic effects of active components of traditional Chinese medicine.Frontiers in pharmacology · 2024Article
- PGK1: A Common Biomarker and Therapeutic Target Linking Sarcopenia and Osteoporosis Through Fibroblast-Mediated Pathways.IET systems biologyArticle
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The prevention of protein condensates has emerged as a new drug target to treat diverse neurodegenerative disorders. We previously reported that terazosin (TZ), a prescribed antagonist of the α1 adrenergic receptor, is an activator of phosphoglycerate kinase 1 (Pgk1) and Hsp90. In this study, we aimed to determine whether TZ prevents the formation of diverse pathological condensates in cell cultures and animal disease models. In primary neuron culture, TZ treatment reduced both the protein density and abundance of fused in sarcoma (FUS)-P525L-GFP, a disease-associated mutant form of FUS. Regarding the mechanism, we found that increased intracellular ATP levels were critical for the reduction in protein aggregate density. In addition, Hsp90 activation by TZ enhanced Hsp90 interaction with ULK1, a master regulator of autophagy. Through in vivo studies, we examined neuron-specific overexpression of tau in Drosophila, mouse models of APP/PS1 Alzheimer's disease (AD), and a rat model of multiple system atrophy (MSA) via the viral expression of α-synuclein in the striatum. TZ prevented and reversed the formation of pathological protein condensates. Together, our results suggest that activation of Pgk1 in cytosol may dissolve pathological protein aggregates via increased ATP levels and degrade these proteins via autophagy; the FUS-P525L degradation pathway in nucleus is unclear.
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