Parkinson’s disease (PD) represents a profoundly enigmatic neurodegenerative ailment marked by the inexorable degradation of dopaminergic neurons. Recent scientific inquiry has brought to the forefront the renin-angiotensin system (RAS) as a central participant within the intricate terrain of PD etiology. The present review endeavors to provide an exhaustive examination of the intricate interrelationship between RAS and PD, elucidating the mechanisms that underlie the harmful progression of this condition. Oxidative stress assumes a central position in PD pathogenesis, and the brain’s RAS, with a focus on Angiotensin II (Ang II), emerges as a catalyst for this phenomenon. Ang II, through AT1 receptors, triggers the production of reactive oxygen species via NADPH oxidase (NOX) enzymes, posing a significant threat to dopaminergic neurons. Moreover, Ang II exerts influence on neuroinflammation, apoptosis, and neurotrophic factors, amplifying neuronal vulnerability. Clinical and pre-clinical evidence underscores the potential of RAS modulators, including ACE inhibitors (ACEIs) and Angiotensin II receptor blockers (ARBs), in mitigating neurodegeneration in PD. These findings offer a promising avenue for novel treatments targeting RAS to protect dopaminergic neurons and alleviate PD symptoms. Natural compounds, specifically flavonoids, have attracted considerable scientific interest as prospective angiotensin-converting enzyme ACEIs. In the future, a deeper understanding of flavonoid metabolism and neuronal access will be instrumental in optimizing their therapeutic potential. Investigating the precise mechanisms by which flavonoids interact with the blood-brain barrier and neuronal tissues may yield innovative treatment strategies for PD.
Key words: Parkinson’s Disease, RAS, Oxidative stress, Neuroinflammation, Flavonoids, ACE
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