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.
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