Description
Title: Parkinson’s Disease and Mitochondrial-Endoplasmic Reticulum Crosstalk: The Function of Brain Renin-Angiotensin System Components
Abstract: The mitochondrial-associated membrane (MAM) has received more attention in recent years due to its potential role in a number of neurodegenerative illnesses, particularly Parkinson’s disease (PD) and Alzheimer’s disease (AD). Protein secretion and metabolism are affected by changes in mitochondrial, endoplasmic reticulum (ER), and MAM functions in PD, which leads to an imbalance in calcium homeostasis and oxidative stress. The translocation of MAM components like IP3R, VDAC, and MFN1 and 2 is altered as a result of these changes, which disturb calcium homeostasis, result in misfolded proteins with impaired autophagy, distorted mitochondrial dynamics, and cell death. According to numerous reports, the brain’s renin-angiotensin system (RAS) negatively affects oxidative stress, neuroinflammation, and apoptosis in a number of neurodegenerative diseases. Using a variety of search engines, including PubMed, SCOPUS, Elsevier, and Springer Nature, we attempted to update the reports in this review that showed the pathogenic interactions between the different proteins present in mitochondria, ER, and MAM with regard to Parkinson’s disease. We also tried to hypothesize the potential role of RAS and its constituents, including AT1 and AT2 receptors and angiotensinogen, in this crosstalk and the pathology of PD. The review compiles and offers up-to-date information on the function of MAM in oxidative stress, neuroinflammation, calcium signaling, and apoptosis in Parkinson’s disease.
Keywords: ER stress; mitochondrial dysfunction; mitochondrial-associated membrane (MAM); ER–mitochondria crosstalk; brain renin angiotensin system
Paper Quality: SCOPUS / Web of Science Level Research Paper
Subject: Biomolecules
Writer Experience: 20+ Years
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