Could Amyloid-beta 1-42 or alpha-Synuclein Interact Directly with Mitochondrial DNA? A Hypothesis

GEZEN AK D., Yurttas Z., Camoglu T., DURSUN E.

ACS CHEMICAL NEUROSCIENCE, vol.13, pp.2803-2812, 2022 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Review
  • Volume: 13
  • Publication Date: 2022
  • Doi Number: 10.1021/acschemneuro.2c00512
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, Chemical Abstracts Core, EMBASE, MEDLINE
  • Page Numbers: pp.2803-2812
  • Keywords: Mitochondrial DNA, mtDNA transcription, amyloid beta, alpha-synuclein, neurodegeneration, mitochondrial dysfunction, Alzheimer's disease, Parkinson disease, ALZHEIMERS-DISEASE, PARKINSONS-DISEASE, VITAMIN-D, GENE-EXPRESSION, COMPLEX-I, PHOSPHORYLATION, TRANSCRIPTION, NEURONS, PROTEIN, MUTATIONS
  • Istanbul University Affiliated: No


The amyloid beta (A beta) and the alpha-synuclein (alpha-syn) are shown to be translocated into mitochondria. Even though their roles are widely investigated in pathological conditions, information on the presence and functions of A beta and alpha-syn in mitochondria in endogenous levels is somewhat limited. We hypothesized that endogenous A beta fragments or alpha-syn could interact with mitochondrial DNA (mtDNA) directly or influence RNAs or transcription factors in mitochondria and change the mtDNA transcription profile. In this review, we summarized clues of these possible interactions.