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, cilt.13, ss.2803-2812, 2022 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Derleme
  • Cilt numarası: 13
  • Basım Tarihi: 2022
  • Doi Numarası: 10.1021/acschemneuro.2c00512
  • Dergi Adı: ACS CHEMICAL NEUROSCIENCE
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, Chemical Abstracts Core, EMBASE, MEDLINE
  • Sayfa Sayıları: ss.2803-2812
  • Anahtar Kelimeler: 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
  • İstanbul Üniversitesi Adresli: Hayır

Özet

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.