Mitochondrial Dynamics and Proteins Related to Neurodegenerative Diseases

Curr Protein Pept Sci. 2018;19(9):850-857. doi: 10.2174/1389203718666170810150151.

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: 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..

Publication types

  • Review

MeSH terms

  • Amyloid beta-Peptides / metabolism*
  • Cell Death
  • Humans
  • Mitochondria / metabolism
  • Mitochondrial Dynamics / physiology*
  • Neurodegenerative Diseases / metabolism*
  • Neurons
  • Protein Conformation
  • Protein Folding
  • Reactive Oxygen Species / metabolism
  • Ubiquitin-Protein Ligases / metabolism
  • alpha-Synuclein / metabolism

Substances

  • Amyloid beta-Peptides
  • Reactive Oxygen Species
  • alpha-Synuclein
  • Ubiquitin-Protein Ligases
  • parkin protein