Abstract
Disruptions in the regulation of mitochondrial dynamics and the occurrence of proteins misfolding lead to neuronal death, resulting in Age-related Dementia and Neurodegenerative diseases as well as Frailty. Functional, neurophysiologic and biochemical alterations within the mitochondrial populations can reveal deficits in brain energy metabolism resulting in Mild Cognitive Impairment, abnormal neural development, autonomic dysfunction and other mitochondrial disorders. Additionally, in cases of Alzheimer’s disease or Parkinson’s disease, a significant number of proteins seem to form unordered and problematic structures, leading through unknown mechanisms to pathological conditions. While the proteins structure prediction problem is still an open challenge regarding its complexity, several features associated with the correlations of misfolding proteins and Neurodegeneration are discussed in the present study and a computational analysis for the proteins Amyloid Beta, Tau, α-Synuclein, Parkin, Pink1, MFN1, MFN1, OPA1, and DNM1L is also presented.
Keywords: Proteins misfolding, mitochondrial dynamics, mitochondrial lesions, neurodegeneration, Alzheimer's disease, Parkinson's disease, Huntington's disease, CMT2A, reactive oxygen species, amyloid beta, tau, α -synuclein, parkin, PINK1, MFN1, MFN2, OPA1, DNM1L.
Current Protein & Peptide Science
Title:Mitochondrial Dynamics and Proteins Related to Neurodegenerative Diseases
Volume: 19 Issue: 9
Author(s): Athanasios Alexiou*, Bilal Nizami, Faez Iqbal Khan, Georgia Soursou, Charalampos Vairaktarakis, Stylianos Chatzichronis, Vasilis Tsiamis, Vasileios Manztavinos, Nagendra Sastry Yarla and Ghulam Md Ashraf*
Affiliation:
- Novel Global Community Educational Foundation, Herbersham,Australia
- King Fahd Medical Research Center, King Abdulaziz University, P.O. Box 80216, Jeddah 21589,Saudi Arabia
Keywords: Proteins misfolding, mitochondrial dynamics, mitochondrial lesions, neurodegeneration, Alzheimer's disease, Parkinson's disease, Huntington's disease, CMT2A, reactive oxygen species, amyloid beta, tau, α -synuclein, parkin, PINK1, MFN1, MFN2, OPA1, DNM1L.
Abstract: Disruptions in the regulation of mitochondrial dynamics and the occurrence of proteins misfolding lead to neuronal death, resulting in Age-related Dementia and Neurodegenerative diseases as well as Frailty. Functional, neurophysiologic and biochemical alterations within the mitochondrial populations can reveal deficits in brain energy metabolism resulting in Mild Cognitive Impairment, abnormal neural development, autonomic dysfunction and other mitochondrial disorders. Additionally, in cases of Alzheimer’s disease or Parkinson’s disease, a significant number of proteins seem to form unordered and problematic structures, leading through unknown mechanisms to pathological conditions. While the proteins structure prediction problem is still an open challenge regarding its complexity, several features associated with the correlations of misfolding proteins and Neurodegeneration are discussed in the present study and a computational analysis for the proteins Amyloid Beta, Tau, α-Synuclein, Parkin, Pink1, MFN1, MFN1, OPA1, and DNM1L is also presented.
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Cite this article as:
Alexiou Athanasios *, Nizami Bilal , Khan Iqbal Faez , Soursou Georgia , Vairaktarakis Charalampos , Chatzichronis Stylianos , Tsiamis Vasilis , Manztavinos Vasileios , Yarla Sastry Nagendra and Ashraf Md Ghulam*, Mitochondrial Dynamics and Proteins Related to Neurodegenerative Diseases, Current Protein & Peptide Science 2018; 19 (9) . https://dx.doi.org/10.2174/1389203718666170810150151
DOI https://dx.doi.org/10.2174/1389203718666170810150151 |
Print ISSN 1389-2037 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5550 |
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