| Literature DB >> 28799502 |
Athanasios Alexiou1, Bilal Nizami2, Faez Iqbal Khan3, Georgia Soursou1, Charalampos Vairaktarakis4, Stylianos Chatzichronis1, Vasilis Tsiamis1,5, Vasileios Manztavinos1,4, Nagendra Sastry Yarla1,6, Ghulam Md Ashraf7.
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. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.Entities:
Keywords: Alzheimer's disease; CMT2A; DNM1L; Huntington's disease; MFN1; MFN2; OPA1; PINK1; Parkinson's disease; Proteins misfolding; amyloid beta; mitochondrial dynamics; mitochondrial lesions; neurodegeneration; parkin; reactive oxygen species; tau; α -synuclein.
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Year: 2018 PMID： 28799502 DOI： 10.2174/1389203718666170810150151
Source DB: PubMed Journal: Curr Protein Pept Sci ISSN： 1389-2037 Impact factor: 3.272