We previously demonstrated that JM-20, a molecule with neuroactive functions, protects rats against rotenone and 6-hydroxydopamine (6-OHDA) neurotoxicity. In addition, we demonstrated that JM-20 inhibits the aggregation and cytotoxicity of alpha-synuclein in vitro. In this study, we performed correlation studies between morphological and molecular variables, as well as the motor behavior of parkinsonian rats (6-OHDA and rotenone lesion) treated with JM-20 at different doses (oral with gavage). Our results showed that higher asymmetry evaluated in the cylinder test correlated with greater redox alterations, death of dopaminergic neurons and increased astrogliosis. In the rotenone model, our results showed that a lower number of vertical rearing was correlated with greater redox alterations and increased mitochondrial dysfunction. In both models (6-OHDA and rotenone), parkinsonian animals treated with the highest doses of JM-20 (20 and 40 mg/kg) showed reduced behavioral impairments (lower asymmetry value and higher amount of vertical rearing). Also, a reduced loss of mesencephalic dopaminergic neurons, a smaller number of astrocyte cells in this region, less redox alterations and less mitochondrial dysfunction was observed. In total, our results demonstrate a correlation between behavioral and biochemical variables evaluated in the preclinical models of parkinsonism induced by 6-OHDA and rotenone.
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http://dx.doi.org/10.1016/j.bbr.2024.115269 | DOI Listing |
Int J Biochem Cell Biol
December 2024
Department of Biochemistry, Faculty of Science, The M.S. University of Baroda, Vadodara, Gujarat 390 002, India. Electronic address:
Parkinson's Disease (PD) is a chronic neurodegenerative disorder that impacts the substantia niagra region of the midbrain leading to impaired motor as well as non-motor symptoms of the central nervous system (CNS). Mitochondrial dysfunction has been characterized as the primary cause of dopaminergic neuronal loss, however, the molecular mechanisms leading to mitochondrial dysfunction are not completely understood. PARKIN, E3 ubiquitin ligase, plays a crucial role in maintaining mitochondrial quality control, albeit the role of other E3 ligases in regulating mitochondrial functions is not understood.
View Article and Find Full Text PDFBehav Brain Res
January 2025
Centro de Investigación y Desarrollo de Medicamentos (CIDEM), Ave 26, No. 1605 Boyeros y Puentes Grandes, La Habana CP 10600, Cuba. Electronic address:
We previously demonstrated that JM-20, a molecule with neuroactive functions, protects rats against rotenone and 6-hydroxydopamine (6-OHDA) neurotoxicity. In addition, we demonstrated that JM-20 inhibits the aggregation and cytotoxicity of alpha-synuclein in vitro. In this study, we performed correlation studies between morphological and molecular variables, as well as the motor behavior of parkinsonian rats (6-OHDA and rotenone lesion) treated with JM-20 at different doses (oral with gavage).
View Article and Find Full Text PDFNeurotoxicology
December 2024
Department of Veterinary Medicine, Federal Rural University of Pernambuco, Brazil.
This systematic review was carried out with the aim of evaluating the use of medicinal Cannabis for the treatment of Parkinson's disease in experimental models. Furthermore, we sought to understand the main intracellular mechanisms capable of promoting the effects of phytocannabinoids on motor disorders, neurodegeneration, neuroinflammation and oxidative stress. The experimental models were developed in mice, rats and marmosets.
View Article and Find Full Text PDFMol Divers
August 2024
Department of Pharmacology, JSS College of Pharmacy, JSS Academy of Higher Education & Research, Ooty, Nilgiris, Tamil Nadu, India.
J Parkinsons Dis
September 2024
Developmental and Regenerative Neurobiology, Department of Experimental Medical Science, Wallenberg Neuroscience Center, Lund University, Lund, Sweden.
Targeted delivery of α-synuclein using AAV vectors has over the two decades since its introduction developed into a versatile tool for modeling different aspects of synucleinopathy, mimicking those seen in Parkinson's disease and related Lewy body disorders. The viral vector approach to disease modeling is attractive in that the expression of α-synuclein, wild-type or mutated, can be confined to defined anatomical structures and targeted to selected cell populations using either cell-type specific promoter constructs or different natural or engineered AAV serotypes. AAV-α-synuclein was initially used to model progressive α-synuclein pathology in nigral dopamine neurons, and, like the standard 6-OHDA model, it has most commonly been applied unilaterally, using the non-injected side as a reference and control.
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