| ABSTRACT |
Background: Disorders like Alzheimer’s and Parkinson’s are defined by the harmful buildup of abnormal proteins namely tau and beta-amyloid in Alzheimer’s, and alpha-synuclein in Parkinson’s accompanied by a gradual decline in nerve cell populations. Growing research suggests that inflammation within the nervous system is not just a byproduct, but plays a central and active role in triggering and sustaining the disease processes in both of these neurological conditions.
Objective: This review seeks to elucidate the contribution of neuroimmune activation to the origins & development of neurodegenerative diseases, pinpoint overlapping and unique inflammatory pathways, and emphasize novel opportunities for therapeutic development.
Methodology: We synthesized recent scientific findings centered on immunological function in both the conditions with special attention to microglial reactivity, NLRP3 inflammasome engagement, disruptions in mitochondrial bioenergetics, and broader systemic immune interactions.
Results: Deposition of beta-amyloid in AD perpetuates sustained microglial activation & escalates the expulsion of inflammation-promoting molecules via NLRP3 inflammasome signaling, culminating in neuronal damage. For Parkinson’s disease, conglomeration of malformed alpha-synuclein intensifies neural cell loss by provoking innate immune defenses and undermining mitochondrial integrity. While each disorder presents distinct clinical features, they converge on shared inflammatory disturbances, including oxidative imbalance, mitochondrial compromise, and irregular cytokine activity.
Discussion: Deposition of beta-amyloid in AD perpetuates sustained microglial activation & escalates the expulsion of inflammation-promoting molecules via NLRP3 inflammasome signaling, culminating in neuronal damage. For Parkinson’s disease, conglomeration of malformed alpha-synuclein intensifies neural cell loss by provoking innate immune defenses and undermining mitochondrial integrity. While each disorder presents distinct clinical features, they converge on shared inflammatory disturbances, including oxidative imbalance, mitochondrial compromise, and irregular cytokine activity.
Conclusion: Diseases like AD & PD are unified by core inflammation cascades but also display disease-specific immunological signatures. Interventions aimed at curbing inflammation such as NLRP3 pathway blockers, anti-inflammatory mediators, and NRF2 pathway modulators hold significant promise for altering disease trajectories. Expanding our understanding of the intricate neuroimmune networks in these disorders may pave the way for innovative neuroprotective therapies. |
| AUTHOR |
Tawqeer Shafi, Bhumi Ruhil1, Khushboo Muzaffar
School of Pharmacy Desh Bhagat University, Mandi Gobindgarh, Punjab, India
Adesh Institute of Pharmacy and Biomedical sciences, Adesh University, Bathinda, Punjab, India |
