Research Journal of Pharmacology and Pharmacodynamics
  • Year: 2026
  • Volume: 18
  • Issue: 1

Cellular and Molecular Mechanisms Contributing to Parkinson’s Disease

  • Author:
  • M Madhuranthagan1, D Benito Johnson1,*, P Essly Selva Jasmine1, R Suresh1, C Senthil Kumar1
  • Total Page Count: 11
  • Page Number: 35 to 45

1Department of Pharmacology, RVS College of Pharmaceutical Sciences, Coimbatore, Tamil Nadu, India

*Corresponding Author E-mail: benitojohnson@rvsgroup.com

Abstract

“Parkinson’s disease” is a long-term, progressively advancing neurological condition marked by motor dysfunction, mainly due to the deterioration of dopamine-secreting “neurons in the substantia nigra pars compacta”. The pathophysiology of is characterized by a marked reduction of dopamine concentration within the basal nuclei, leading to classic movement-related symptoms such as slowness of movement, quivering, firmness, and loss of balance. At the cellular level, PD is associated with the conglomeration of mis organize α-synuclein polypeptides, forming Lewy bodies, which are considered a tell-tale sign of the illness. Mitochondrial dysfunction, oxidative stress, impaired protein degradation systems (namely Proteolytic pathway driven by ubiquitin labeling and proteasomal cleavage), and neuroinflammation contribute to neuronal damage. Genetic alterations in genes like SNCA, LRRK2, PARK2, and PINK1 significantly contribute to Lineage-associated and isolated occurrences of the disease. Understanding the complex pathophysiology of Insights into PD are fundamental for the development of disease-modifying therapies with the objective of halting or reversing neurodegeneration beyond symptomatic management. Emerging research has identified novel biomarkers for early detection, including volatile compounds in earwax, RNA signatures in blood, and motor patterns captured via smart devices. These developments hold promise for pre-symptomatic diagnosis and personalized monitoring. In parallel, studies suggest a possible viral trigger—human pegivirus (HPgV)—that may act synergistically with genetic mutations (e.g., LRRK2), redefining disease etiology. Therapeutic innovations include disease-modifying strategies such as targeted gene therapy (e.g., AAV2-GDNF), patient-derived stem cell transplantation, and misfolded protein correction (SOD1-related pathways). Additionally, symptomatic relief through neuromodulation, dopamine receptor agonists, and psychedelic-assisted therapy (e.g., psilocybin) offer improved quality of life for patients. Collectively, these multi-disciplinary advances—spanning virology, genetics, neurotechnology, and pharmacology—are converging toward a transformative approach for managing and potentially overcoming “Parkinson’s disease”. Ongoing clinical trials and integrative diagnostic systems will be critical in translating these findings into routine care.

Keywords

α-Synuclein, Parkin, Mitochondrial Complex-I, Ubiquitin-proteasome system, Oxidative stress, Autophagy, Neuroinflammation