ArticleNeurotoxicity research2012
Dimebon slows progression of proteinopathy in γ-synuclein transgenic mice.
Article in Neurotoxicity research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 41 citations in OpenAlex.
- Therapeutic Potential of Heterocyclic Compounds Targeting Mitochondrial Calcium Homeostasis and Signaling in Alzheimer's Disease and Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2023Review
- A bioisostere of Dimebon/Latrepirdine delays the onset and slows the progression of pathology in FUS transgenic mice.CNS neuroscience & therapeutics · 2021Article
- Mitochondrial Pharmacology of Dimebon (Latrepirdine) Calls for a New Look at its Possible Therapeutic Potential in Alzheimer's Disease.Aging and disease · 2018Review
- Pro-neurogenic, Memory-Enhancing and Anti-stress Effects of DF302, a Novel Fluorine Gamma-Carboline Derivative with Multi-target Mechanism of Action.Molecular neurobiology · 2018Article
- Phosphorylation of the Amyloid-Beta Peptide Inhibits Zinc-Dependent Aggregation, Prevents Na,K-ATPase Inhibition, and Reduces Cerebral Plaque Deposition.Frontiers in molecular neuroscience · 2018Article
- Detection of autoantibodies to potentially amyloidogenic protein, gamma-synuclein, in the serum of patients with amyotrophic lateral sclerosis and cerebral circulatory disorders.Doklady. Biochemistry and biophysics · 2017Article
- Actions of the antihistaminergic clemastine on presymptomatic SOD1-G93A mice ameliorate ALS disease progression.Journal of neuroinflammation · 2016Article
- Intracerebral Injection of Metal-Binding Domain of Aβ Comprising the Isomerized Asp7 Increases the Amyloid Burden in Transgenic Mice.Neurotoxicity research · 2016Article
- The Effects of Latrepirdine on Amyloid-β Aggregation and Toxicity.Journal of Alzheimer's disease : JAD · 2016Article
- Novel Sites of Neuroprotective Action of Dimebon (Latrepirdine).Molecular neurobiology · 2015Review
- Gamma-carboline inhibits neurodegenerative processes in a transgenic model of amyotrophic lateral sclerosis.Doklady. Biochemistry and biophysics · 2015Article
- Latrepirdine: molecular mechanisms underlying potential therapeutic roles in Alzheimer's and other neurodegenerative diseases.Translational psychiatry · 2013Review
- Peripherally applied synthetic peptide isoAsp7-Aβ(1-42) triggers cerebral β-amyloidosis.Neurotoxicity research · 2013Article
- Latrepirdine stimulates autophagy and reduces accumulation of α-synuclein in cells and in mouse brain.Molecular psychiatry · 2013Article
- The age-related gliosis and accompanying deficit in spatial learning are unaffected by dimebon.Neurochemical research · 2013Article
- Latrepirdine (dimebon) enhances autophagy and reduces intracellular GFP-Aβ42 levels in yeast.Journal of Alzheimer's disease : JAD · 2012Article
- Article
- Dimebon activates autophagosome components in human neuroblastoma SH-SY5Y cells.Doklady. Biochemistry and biophysicsArticle
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Intermediates and final products of protein aggregation play crucial role in the development of degenerative changes in a number of neurological diseases. Pathological protein aggregation is currently regarded as one of the most promising therapeutic targets for treatment of these diseases. Transgenic mouse models of proteinopathies are an effective tool for screening and validation of compounds, which can selectively affect metabolism of aggregate-prone proteins. In this study, we assessed effects of dimebon, a compound with known neuroprotective properties, on a recently established transgenic mouse model recapitulating key pathological features of amyotrophic lateral sclerosis (ALS) as the consequence of neuron-specific overexpression of γ-synuclein. Cohorts of experimental transgenic mice received dimebon in drinking water with this chronic treatment starting either before or after the onset of clinical signs of pathology. We detected statistically significant improvement of motor performance in a rotarod test in both dimebon-treated animal groups, with more pronounced effect in a group that received dimebon from an earlier age. We also revealed substantially reduced number of amyloid inclusions, decreased amount of insoluble γ-synuclein species and a notable amelioration of astrogliosis in the spinal cord of dimebon-treated compared with control transgenic animals. However, dimebon did not prevent the loss of spinal motor neurons in this model. Our results demonstrated that chronic dimebon administration is able to slow down but not halt progression of γ-synucleinopathy and resulting signs of pathology in transgenic animals, suggesting potential therapeutic use of this drug for treatment of this currently incurable disease.
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Registered trials
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.