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

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Dietary Caffeic Acid Exhibits Neuroprotective and Neuromodulatory Effects in a Parkinsonian Rat Model by Mitigating Oxidative Stress, Mitochondrial Dysfunction, and Apoptosis

A. Singh (Prayagraj, India)

Meeting: 2025 International Congress

Keywords: 1-Methyl-4-phenylpyridinium (MPP+), Dopaminergic neurons, Parkinson’s

Category: Parkinson’s Disease: Pharmacology and Medical Management

Objective: This study investigated the neuroprotective and neuromodulatory effects of dietary caffeic acid (CA) in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinsonian rat model

Background: Parkinson’s disease (PD) is a neurodegenerative disorder characterized by motor dysfunction, primarily due to the degeneration of dopaminergic neurons in the substantia nigra. Mitochondrial dysfunction, oxidative stress, and neuronal apoptosis are central to PD pathogenesis. Current therapies focus on symptom management, but no definitive cure exists. Phytochemicals, such as CA, have gained attention for their antioxidant and anti-inflammatory properties, offering potential therapeutic benefits.

Method: Rats were divided into three groups: normal, MPTP control, and MPTP+CA. CA was administered orally for 28 days. Weekly assessments included body weight and locomotor behavior (rotarod performance, hanging test, and narrow beam traversal time). Post-experiment, brain samples were analyzed for mitochondrial complex activity, antioxidant levels (SOD, catalase, glutathione), apoptotic protein expression (caspase-3, Bax, Bcl-2), and inflammatory cytokines (IL-1β, TNF-α).

Results: MPTP-intoxicated rats exhibited impaired motor coordination, reduced mitochondrial complex activity, elevated oxidative stress, and increased apoptosis. CA treatment significantly improved locomotor performance, enhanced mitochondrial function, and increased antioxidant enzyme levels. CA also downregulated proapoptotic proteins (caspase-3, Bax) and upregulated antiapoptotic Bcl-2, while reducing inflammatory markers (IL-1β, TNF-α).

Conclusion: Dietary CA mitigates oxidative stress, mitochondrial dysfunction, and apoptosis in MPTP-induced Parkinsonian rats, suggesting its potential as a therapeutic agent for neurodegenerative disorders. Further studies are warranted to validate its efficacy and elucidate underlying molecular mechanisms in clinical settings.

To cite this abstract in AMA style:

A. Singh. Dietary Caffeic Acid Exhibits Neuroprotective and Neuromodulatory Effects in a Parkinsonian Rat Model by Mitigating Oxidative Stress, Mitochondrial Dysfunction, and Apoptosis [abstract]. Mov Disord. 2025; 40 (suppl 1). https://www.mdsabstracts.org/abstract/dietary-caffeic-acid-exhibits-neuroprotective-and-neuromodulatory-effects-in-a-parkinsonian-rat-model-by-mitigating-oxidative-stress-mitochondrial-dysfunction-and-apoptosis/. Accessed October 5, 2025.
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MDS Abstracts - https://www.mdsabstracts.org/abstract/dietary-caffeic-acid-exhibits-neuroprotective-and-neuromodulatory-effects-in-a-parkinsonian-rat-model-by-mitigating-oxidative-stress-mitochondrial-dysfunction-and-apoptosis/

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