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Proteinopathy, oxidative stress and mitochondrial dysfunction: cross talk in Alzheimer's disease and Parkinson's disease.
Drug Des Devel Ther. 2017; 11:797-810.DD

Abstract

Alzheimer's disease and Parkinson's disease are two common neurodegenerative diseases of the elderly people that have devastating effects in terms of morbidity and mortality. The predominant form of the disease in either case is sporadic with uncertain etiology. The clinical features of Parkinson's disease are primarily motor deficits, while the patients of Alzheimer's disease present with dementia and cognitive impairment. Though neuronal death is a common element in both the disorders, the postmortem histopathology of the brain is very characteristic in each case and different from each other. In terms of molecular pathogenesis, however, both the diseases have a significant commonality, and proteinopathy (abnormal accumulation of misfolded proteins), mitochondrial dysfunction and oxidative stress are the cardinal features in either case. These three damage mechanisms work in concert, reinforcing each other to drive the pathology in the aging brain for both the diseases; very interestingly, the nature of interactions among these three damage mechanisms is very similar in both the diseases, and this review attempts to highlight these aspects. In the case of Alzheimer's disease, the peptide amyloid beta (Aβ) is responsible for the proteinopathy, while α-synuclein plays a similar role in Parkinson's disease. The expression levels of these two proteins and their aggregation processes are modulated by reactive oxygen radicals and transition metal ions in a similar manner. In turn, these proteins - as oligomers or in aggregated forms - cause mitochondrial impairment by apparently following similar mechanisms. Understanding the common nature of these interactions may, therefore, help us to identify putative neuroprotective strategies that would be beneficial in both the clinical conditions.

Authors+Show Affiliations

Department of Pathology, Institute of Post Graduate Medical Education and Research, Kolkata.Department of Biochemistry, ICARE Institute of Medical Sciences and Research, Haldia, West Bengal, India.Department of Pathology, Institute of Post Graduate Medical Education and Research, Kolkata.Department of Physiology and Pharmacology "Vittorio Erspamer", Sapienza University of Rome, Rome, Italy.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

28352155

Citation

Ganguly, Gargi, et al. "Proteinopathy, Oxidative Stress and Mitochondrial Dysfunction: Cross Talk in Alzheimer's Disease and Parkinson's Disease." Drug Design, Development and Therapy, vol. 11, 2017, pp. 797-810.
Ganguly G, Chakrabarti S, Chatterjee U, et al. Proteinopathy, oxidative stress and mitochondrial dysfunction: cross talk in Alzheimer's disease and Parkinson's disease. Drug Des Devel Ther. 2017;11:797-810.
Ganguly, G., Chakrabarti, S., Chatterjee, U., & Saso, L. (2017). Proteinopathy, oxidative stress and mitochondrial dysfunction: cross talk in Alzheimer's disease and Parkinson's disease. Drug Design, Development and Therapy, 11, 797-810. https://doi.org/10.2147/DDDT.S130514
Ganguly G, et al. Proteinopathy, Oxidative Stress and Mitochondrial Dysfunction: Cross Talk in Alzheimer's Disease and Parkinson's Disease. Drug Des Devel Ther. 2017;11:797-810. PubMed PMID: 28352155.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Proteinopathy, oxidative stress and mitochondrial dysfunction: cross talk in Alzheimer's disease and Parkinson's disease. AU - Ganguly,Gargi, AU - Chakrabarti,Sasanka, AU - Chatterjee,Uttara, AU - Saso,Luciano, Y1 - 2017/03/16/ PY - 2017/3/30/entrez PY - 2017/3/30/pubmed PY - 2017/5/16/medline KW - amyloid beta KW - mitochondrial dysfunction KW - oxidative stress KW - proteinopathy KW - α-synuclein SP - 797 EP - 810 JF - Drug design, development and therapy JO - Drug Des Devel Ther VL - 11 N2 - Alzheimer's disease and Parkinson's disease are two common neurodegenerative diseases of the elderly people that have devastating effects in terms of morbidity and mortality. The predominant form of the disease in either case is sporadic with uncertain etiology. The clinical features of Parkinson's disease are primarily motor deficits, while the patients of Alzheimer's disease present with dementia and cognitive impairment. Though neuronal death is a common element in both the disorders, the postmortem histopathology of the brain is very characteristic in each case and different from each other. In terms of molecular pathogenesis, however, both the diseases have a significant commonality, and proteinopathy (abnormal accumulation of misfolded proteins), mitochondrial dysfunction and oxidative stress are the cardinal features in either case. These three damage mechanisms work in concert, reinforcing each other to drive the pathology in the aging brain for both the diseases; very interestingly, the nature of interactions among these three damage mechanisms is very similar in both the diseases, and this review attempts to highlight these aspects. In the case of Alzheimer's disease, the peptide amyloid beta (Aβ) is responsible for the proteinopathy, while α-synuclein plays a similar role in Parkinson's disease. The expression levels of these two proteins and their aggregation processes are modulated by reactive oxygen radicals and transition metal ions in a similar manner. In turn, these proteins - as oligomers or in aggregated forms - cause mitochondrial impairment by apparently following similar mechanisms. Understanding the common nature of these interactions may, therefore, help us to identify putative neuroprotective strategies that would be beneficial in both the clinical conditions. SN - 1177-8881 UR - https://www.unboundmedicine.com/medline/citation/28352155/Proteinopathy_oxidative_stress_and_mitochondrial_dysfunction:_cross_talk_in_Alzheimer's_disease_and_Parkinson's_disease_ L2 - https://dx.doi.org/10.2147/DDDT.S130514 DB - PRIME DP - Unbound Medicine ER -