Parkinsonism represents a spectrum of neuro-degenerative disorders hallmarked by progressive motor symptoms, with a growing recognition of diverse non-motor manifestations that significantly affects quality of life. The understanding of Parkinson’s disease is changing, with growing evidence showing that the gut-brain-axis is the communication link between the gut, brain, immune system, and gut microbes and plays an important role in how the disease starts and develops.This literature review systematically evaluates research published post-2020, focusing on mechanistic insights, clinical significance, and therapeutic possibilities of gut–brain axis modulation in parkinsonism. Database searches across PubMed and Google Scholar yielded 70 articles, with 29 English-language, full-text studies selected, emphasizing relevance to gut microbiota, intestinal barrier dysfunction, neuro-inflammatory mechanisms, and interventions targeting the GBA.Key findings highlight that early gastrointestinal dysfunction Precedes by many years before the classical motor symptoms appear in Parkinsonism. Accumulation of misfolded alpha-synuclein in enteric neurons supports the Braak's hypothesis of peripheral origin and vagus nerve-mediated propagation to the brain, supported by the detection of Lewy pathology in gut tissues and experimental evidence from animal models. The “leaky gut” phenomenon is shown to trigger systemic and neuroinflammation, further facilitating alpha-syn aggregation and neuro-degeneration. Dysbiosis is consistently observed in many studies, marked by reduced diversity and diminished populations of SCFA producing bacteria (Prevotella, Faecalibacterium, Roseburia) with corresponding expansion of pro-inflammatory taxa (Akkermansia, Lactobacillus, Enterococcus, Desulfovibrio). Environmental and lifestyle factors—including Western dietary patterns, infections, pesticides, and chronic stress—contribute to the worsening of microbiota profiles and gut barrier function, whereas adoption of Mediterranean or vegetarian diets improvesmicrobial diversity and could decrease disease risk or progression. “Body-first” and “brain-first” pathophysiological subtypes of PD are found to differentiate cases where alpha-synuclein pathology either starts peripherally and spreads centrally or originates in the brain itself, indicating tailored clinical approaches required.Therapeutically, advances in probiotics, prebiotics, fiber-rich dietary strategies, FMT, and innovative pharmacological or neuromodulatory interventions (including GLP-1 agonists, nutraceuticals, and vagus nerve stimulation) offer promising results but still need further research to increase efficacy . Despite exciting progress, several limitations constrain the field: the absence of definitive causal relationships, substantial inter-individual microbiome variability, and short-term, small-scale clinical studies. Biomarker development and clinical translation are hindered by population heterogeneity and methodological inconsistencies. Future research must focus on longitudinal designs tracking microbiota dynamics from early stages, mechanistic clarity of bidirectional GBA signaling, and combination therapies that combine lifestyle, dietary, and advanced medical approaches for optimized patient outcomes.