Parkinson disease Scientific Publications

Latest publication 03/25/2026

Urolithin A Reverses Intranigral Rotenone-Generated Parkinsonism by Modulating D

Epigenetic aberrations play a key role in the neuropathogenesis of Parkinson’s disease (PD). Herein, we explored the post-translational changes of...

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    [title] => Urolithin A Reverses Intranigral Rotenone-Generated Parkinsonism by Modulating D
    [paragraph] => Urolithin A Reverses Intranigral Rotenone-Generated Parkinsonism by Modulating DNA Methyltransferase 1 and α-Synuclein Axis in Rats | ACS Chemical Neuroscience
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Authors
Ankita  Devi, Shashi Bala  Singh, Saurabh  Srivastava, Manoj P.  Dandekar

Lab
Brought to you by ACS Institute
Journal
ACS Chemical Neuroscience
Abstract
Epigenetic aberrations play a key role in the neuropathogenesis of Parkinson’s disease (PD). Herein, we explored the post-translational changes of DNA methyltransferase 1 (DNMT1), an epigenetic marker, in a rotenone model of PD. Rats infused with intranigral rotenone showed impaired locomotor activity and motor coordination in open-field, rotarod, and gait assays. We also noted a depression-like phenotype in the forced swim test (FST). These rotenone-generated motor and nonmotor abnormalities were reversed following peroral administration of urolithin A (UA) at 50 and 100 mg/kg doses. At the molecular level, decreased mRNA/protein expression of the NAD+-dependent sirtuin 1 (SIRT1) enzyme was seen in the substantia nigra (SN) of the rotenone-infused group. At the epigenetic level, we observed a decreased expression of DNMT1 and upregulated levels of acetylated DNMT1 (ac-DNMT1) in the SN of rotenone-recipient rats. UA treatment elevated the SIRT1 expression and DNMT1 deacetylation in the SN of rotenone-lesioned rats. However, DNMT1 mRNA expression remained unchanged across the groups. Thein-silicobinding of the catalytic region of SIRT1 to DNMT1 (over the BAH2 and catalytic domains) and its stability over a 300 ns simulation indicated the importance of SIRT1 in deacetylating DNMT1 protein. This led to UA-mediated elevation of 5-methylcytosine (5-mC) levels, promoting global DNA hypermethylation in the SN and alpha-synuclein (SNCA) promoter region methylation in the striatum. UA treatment also downregulated the SNCA gene expression and α-synuclein levels in rotenone-lesioned rats. These findings indicate that UA treatment may reverse rotenone-induced PD progression through modulation of the SIRT1/ac-DNMT1/5-mC axis within the neuroanatomical framework of the SN.
Keywords/Topics
Parkinson’s disease; urolithin A; rotenone; DNMT1 acetylation; hypomethylation; substantia nigra
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Rotarod provides an easy way to test the motor activity in rodents (mouse or rat) - an ideal solution for studying central nervous system damage, disease effects on motor activity, drugs administration, fatigue resistance, etc. Now even easier to use! The new touchscreen graphic user interface allows clear visualization of timing and speed for each lane. Change modes, adjust speed, and create protocols right from the main screen for greater flexibility with maximum functionality and usability

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