Volume 10 ; Issue 1 ; in Month : Jan-June (2026) Article No : 200
Shoba S, Nishvanth F, Kiruthika K, et al.

Abstract

Parkinson’s disease (PD) is the second most common neurodegenerative disorder and the fastest-growing neurological condition worldwide. It is primarily characterized by motor symptoms such as bradykinesia, rigidity, resting tremor, and postural instability, resulting from the progressive loss of dopaminergic neurons in the substantia nigra pars compacta. Non-motor symptoms—including sleep disturbances, constipation, urinary dysfunction, cognitive decline, and mood disorders—often develop years before motor onset, reflecting PD’s multisystem involvement. The underlying pathophysiology involves complex interactions of genetic, environmental, and aging-related factors that contribute to mitochondrial dysfunction, oxidative stress, α-synuclein aggregation, impaired autophagy-lysosomal pathways, and neuro-inflammation. Mutations in genes such as SNCA, LRRK2, PRKN, PINK1, and GBA1 further highlight the role of genetic susceptibility. Environmental exposures, including pesticides and heavy metals, also increase risk, while factors like caffeine and smoking appear protective. Current diagnosis relies heavily on clinical features, supported by emerging biomarkers and neuroimaging techniques that detect early dopaminergic deficits. Although no disease-modifying therapies exist, advancements in understanding PD’s molecular mechanisms are driving the development of novel therapeutic strategies, including gene therapy, neuroprotective agents, and personalized medicine approaches. Early identification through prodromal markers may be key to enabling effective intervention and slowing disease progression.

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