TY - JOUR
T1 - Mitochondrial dynamics and proteins related to neurodegenerative diseases
AU - Alexiou, Athanasios
AU - Nizami, Bilal
AU - Khan, Faez Iqbal
AU - Soursou, Georgia
AU - Vairaktarakis, Charalampos
AU - Chatzichronis, Stylianos
AU - Tsiamis, Vasilis
AU - Manztavinos, Vasileios
AU - Yarla, Nagendra Sastry
AU - Md Ashraf, Ghulam
N1 - Publisher Copyright:
© 2018 Bentham Science Publishers.
PY - 2018
Y1 - 2018
N2 - 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.
AB - 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.
KW - Alzheimer’s disease
KW - Amyloid beta
KW - CMT2A
KW - DNM1L
KW - Huntington's disease
KW - MFN1
KW - MFN2
KW - Mitochondrial dynamics
KW - Mitochondrial lesions
KW - Neurodegeneration
KW - OPA1
KW - PINK1
KW - Parkin
KW - Parkinson’s disease
KW - Proteins misfolding
KW - Reactive oxygen species
KW - Tau
KW - α-synuclein
UR - http://www.scopus.com/inward/record.url?scp=85048345773&partnerID=8YFLogxK
U2 - 10.2174/1389203718666170810150151
DO - 10.2174/1389203718666170810150151
M3 - Review article
C2 - 28799502
AN - SCOPUS:85048345773
SN - 1389-2037
VL - 19
SP - 850
EP - 857
JO - Current Protein and Peptide Science
JF - Current Protein and Peptide Science
IS - 9
ER -