Targeting the overexpressed mitochondrial protein vdac1 in a mouse model of alzheimer’s disease protects against mitochondrial dysfunction and mitigates brain pathology

HIGHLIGHTS

• who: Ankit Verma from the Male , u00d7 FAD transgenic mice were obtained from the Jackson Laboratory (Bar Harbor, ME) and crossed with C Bl/RCC female miceThe , u00d7 FAD transgenic mice have five familial AD mutations, including amyloid precursor protein (APP) with K N/M L (Swedish mutation), I V (Florida mutation), and V I (London mutation), and presenilin , (PS1) with M L and L V mutations ([, u00d7 FAD, .Cg-TgAPPSwFlLon, PSEN1*M Ln *L , Vas/J]). These mice develop massive cerebral Au03b2, loads, memory deficits, and neuronal loss [45]. Male offspring were genotyped by PCR analysis . . .
  

   

  

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