MDS Abstracts

Abstracts from the International Congress of Parkinson’s and Movement Disorders.

MENU 
  • Home
  • Meetings Archive
    • All Meetings
    • 2026 International Congress
  • Keyword Index
  • Resources
  • Advanced Search

PPAR-γ-dependent Neuroprotection by Ferulic acid improves Motor deficits in 3-nitropropionic acid model of Huntington’s disease in rats

N. Singh, V. Singh (bathinda, India)

Meeting: 2026 International Congress

Keywords: Chorea (also see specific diagnoses, Huntingtons disease, etc): Treatment, Mitochondrial dysfunction, Neuroprotective agents

Category: Huntington's Disease

Objective: This study investigates the neuroprotective role of FA in  3-nitropropionic acid (3-NP) model of HD through PPAR-γ–mediated mechanisms.

Background: Huntington disease (HD) is a neurodegenerative disorder, characterized by progressive motor impairments, caused by a number of processes, including oxidative stress, neurotransmitter imbalance, mitochondrial dysfunction and excitotoxicity. Peroxisome proliferator-activated receptor-γ (PPAR-γ) is a key transcriptional regulator of these pathways. Ferulic acid (FA), a natural phenolic compound, has strong antioxidant and anti-inflammatory activities, even though the reports revealing the associated mechanism of action against HD are scanty.

Method: Rats received 3-NP (10 mg/kg, i.p.) for 21 days to induce neurodegeneration, followed by oral FA treatment (40 and 80 mg/kg once daily). BADGE, a PPAR-γ inhibitor (15 mg/kg) was also used to highlight the role of PPAR-γ pathway. Behaviour parameter included open field test, grip strength, test narrow beam walk, and rotarod tests while biochemical parameters quantified inflammatory markers (TNF-α, NF-κB, IL-1β, IL-6), oxidative stress markers (GSH, TBARS), and mitochondrial complex I–IV activities, alongside histopathological assessment (H&E staining) for neuronal integrity.

Results: FA treatment markedly enhanced motor functions, suppressed neuroinflammatory cytokines, restored redox balance, and normalized mitochondrial complex I–IV activities, corroborated by preservation of neuronal architecture. Importantly, co-administration of BADGE, a PPAR-γ inhibitor, markedly abolished the behavioral and biochemical benefits of FA, confirming the pivotal role of PPAR-γ activation in its neuroprotective mechanism.

Conclusion: These findings demonstrate that PPAR-γ modulation by ferulic acid, act as a promising strategy for managing Huntington Disease.

To cite this abstract in AMA style:

N. Singh, V. Singh. PPAR-γ-dependent Neuroprotection by Ferulic acid improves Motor deficits in 3-nitropropionic acid model of Huntington’s disease in rats [abstract]. Mov Disord. 2026; 41 (suppl 1). https://www.mdsabstracts.org/abstract/ppar-%ce%b3-dependent-neuroprotection-by-ferulic-acid-improves-motor-deficits-in-3-nitropropionic-acid-model-of-huntingtons-disease-in-rats/. Accessed October 1, 2026.
  • Tweet
  • Email a link to a friend (Opens in new window) Email
  • Print (Opens in new window) Print

« Back to 2026 International Congress

MDS Abstracts - https://www.mdsabstracts.org/abstract/ppar-%ce%b3-dependent-neuroprotection-by-ferulic-acid-improves-motor-deficits-in-3-nitropropionic-acid-model-of-huntingtons-disease-in-rats/

Related Sites

International Parkinson and Movement Disorder Society

The Society that manages the annual International Congress »

International Congress

The official website for the International Congress of Parkinson’s and Movement Disorders® »

  • Help & Support
  • About Us
  • Cookies & Privacy
  • Wiley Job Network
  • Terms & Conditions
  • Advertisers & Agents
Copyright © 2026 International Parkinson and Movement Disorder Society. All Rights Reserved.
Wiley