Mitigating neuroinflammation in Parkinson's disease: Exploring the role of proinflammatory cytokines and the potential of phytochemicals as natural therapeutics.

Parkinson's disease (PD) is one of the most prevalent neuroinflammatory illnesses, characterized by the progressive loss of neurons in the brain. Proinflammatory cytokines play a key role in initiating and perpetuating neuroinflammation, which can lead to the activation of glial cells and the deregulation of inflammatory pathways, ultimately leading to permanent brain damage. Currently, available drugs for PD mostly alleviate symptoms but do not target underlying inflammatory processes. There is a growing interest in exploring the potential of phytochemicals to mitigate neuroinflammation. Phytochemicals such as resveratrol, apigenin, catechin, anthocyanins, amentoflavone, quercetin, berberine, and genistein have been studied for their ability to scavenge free radicals and reduce proinflammatory cytokine levels in the brain. These plant-derived compounds offer a natural and potentially safe alternative to conventional drugs for managing neuroinflammation in PD and other neurodegenerative diseases. However, further research is necessary to elucidate their underlying mechanisms of action and clinical effectiveness. So, this review delves into the pathophysiology of PD and its intricate relationship with proinflammatory cytokines, and explores how their insidious contributions fuel the disease's initiation and progression via cytokine-dependent signaling pathways. Additionally, we tried to give an account of PD management using existing drugs along with their limitations. Furthermore, our aim is to provide a thorough overview of the diverse groups of phytochemicals, their plentiful sources, and the current understanding of their anti-neuroinflammatory properties. Through this exploration, we posit the innovative idea that consuming nutrient-rich phytochemicals could be an effective approach to preventing and treating PD.

The role of fatty acid amide hydrolase enzyme inhibitors in Alzheimer's disease.

Fatty acid amide hydrolase (FAAH) is a prominent enzyme of the endocannabinoid system that degrades endogenous cannabinoid anandamide and oleamide. These lipid amides are involved in reducing neuroinflammation, pain and regulation of other neurological-related activities including feeding behaviours, sleep patterns, body temperature, memory processes and locomotory activity. Many of these activities are affected in most neurological disorders. Increased levels of brain FAAH expressions are speculated to correlate with decreased levels of lipid amides and increased AD-related symptoms. Thus, inhibition of FAAH shows promising potential in amelioration of symptoms associated with Alzheimer's disease (AD). The review aims at establishing the detrimental role of increased FAAH expression in AD and highlights the translational potential and therapeutic application of FAAH inhibitors in AD.