ArticleACS chemical neuroscience2013
Restoration of glyoxalase enzyme activity precludes cognitive dysfunction in a mouse model of Alzheimer's disease.
Article in ACS chemical neuroscience, 2013. 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, 54 citations in OpenAlex.
- Rational Design of an Electronically Gated Dicyano-BODIPY Platform for Reversible-Covalent Imaging of Methylglyoxal.JACS Au · 2026Article
- Spin-driven enantioselective regulation of cyclooxygenase-2 activity for rheumatoid arthritis therapy via chiral gold nanohelices.Nature communications · 2026Article
- Living Cells Employ Ubiquitin-Proteasomal System and Nucleotide Excision Repair Pathways to Remove Reactive Oxygen Species-Induced DNA-Protein Crosslinks (ROS-DPCs).bioRxiv : the preprint server for biology · 2026Article
- Deep learning identifies TP-41 for methylglyoxal scavenging in Alzheimer's treatment.Theranostics · 2026Article
- Oral Prodrug of a Novel Glutathione Surrogate Reverses Metabolic Dysregulation and Attenuates Neurodegenerative Process in Transgenic Alzheimer's Mice.ACS pharmacology & translational science · 2025Article
- Deletion of Glyoxalase 1 exacerbates acetaminophen-induced hepatotoxicity in mice.bioRxiv : the preprint server for biology · 2023Article
- Role of neuroinflammation in neurodegeneration development.Signal transduction and targeted therapy · 2023Review
- Orally Bioavailable Prodrugs of ψ-GSH: A Potential Treatment for Alzheimer's Disease.Journal of medicinal chemistry · 2022Article
- Design of an activatable NIR-II nanoprobe for theChemical science · 2022Article
- Dipeptide of ψ-GSH Inhibits Oxidative Stress and Neuroinflammation in an Alzheimer's Disease Mouse Model.Antioxidants (Basel, Switzerland) · 2022Article
- γ-Glutamyl-Transpeptidase-Resistant Glutathione Analog Attenuates Progression of Alzheimer's Disease-like Pathology and Neurodegeneration in a Mouse Model.Antioxidants (Basel, Switzerland) · 2021Article
- Vescalagin from Pink Wax Apple (Plants (Basel, Switzerland) · 2021Article
- Sulfur-containing therapeutics in the treatment of Alzheimer's disease.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2021Article
- CDH6 and HAGH protein levels in plasma associate with Alzheimer's disease in APOE ε4 carriers.Scientific reports · 2020Article
- Cerebral microvascular complications of type 2 diabetes: stroke, cognitive dysfunction, and depression.The lancet. Diabetes & endocrinology · 2020Review
- 20S proteasome and glyoxalase 1 activities decrease in erythrocytes derived from Alzheimer's disease patients.Neural regeneration research · 2020Article
- Increased expression of heme-binding protein 1 early in Alzheimer's disease is linked to neurotoxicity.eLife · 2019Article
- Review
- Article
- Neuroprotection through flavonoid: Enhancement of the glyoxalase pathway.Redox biology · 2018Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pathologically high brain levels of reactive dicarbonyls such as methylglyoxal or glyoxal initiate processes that lead ultimately to neurodegeneration, presented clinically as Alzheimer's disease and other cognitive or motor impairment disorders. Methylglyoxal and glyoxal result from glycolysis and normal metabolic pathways. Their reaction products with proteins (advanced glycation end products), and their primary chemical toxicities are both linked unequivocally to the primary pathologies of Alzheimer's disease, namely, amyloid plaques and neurofibrillary tangles. Generation of dicarbonyls is countered through the reduction of dicarbonyls by the glutathione-dependent glyoxalase enzyme system. Although glyoxalase-I is overexpressed in early and middle stages of Alzheimer's disease, glutathione depletion in the Alzheimer's afflicted brain cripples its efficacy. Due to the lack of a suitable pharmacological tool, the restoration of glyoxalase enzyme activity in pre-Alzheimer's or manifest Alzheimer's remains yet unvalidated as a means for anti-Alzheimer's therapy development. Disclosed herein are the results of a preclinical study into the therapeutic efficacy of ψ-GSH, a synthetic cofactor of glyoxalase, in mitigating Alzheimer's indicators in a transgenic mouse model (APP/PS1) that is predisposed to Alzheimer's disease. ψ-GSH administration completely averts the development of spatial mnemonic and long-term cognitive/cued-recall impairment. Amyloid β deposition and oxidative stress indicators are drastically reduced in the ψ-GSH-treated APP/PS1 mouse. ψ-GSH lacks discernible toxicity at strikingly high doses of 2000 mg/kg. The hypothesis that restoring brain glyoxalase activity would ameliorate neurogeneration stands validated, thus presenting a much needed new target for design of anti-Alzheimer's therapeutics. Consequently, ψ-GSH is established as a candidate for drug-development.
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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.