No abstract

The amyloid β (Aβ) and the α-synuclein (α-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 Aβ and α-syn in mitochondria in endogenous levels is somewhat limited. We hypothesized that endogenous Aβ fragments or α-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.