title: Hypoxia-up-regulated mitochondrial movement regulator does not contribute to the APP/PS1 double transgenic mouse model of Alzheimer's disease.
abstract: OBJECTIVE
  It has been demonstrated that mitochondrial dysfunction is associated with Alzheimer's disease (AD); meanwhile, hypoxia-up-regulated mitochondrial movement regulator (HUMMR) plays an important role in regulating mitochondrial function. The present study aimed to confirm the association between HUMMR and mitochondrial function in AD.
  
  
  METHODS
  We detected the expression of HUMMR at transcriptional and translational levels in APP/PS1 double transgenic mice using real-time quantitative RT-PCR and Western blotting. Age- and gender-matched wild-type (WT) littermates were used as controls. Mitochondrial morphology was observed in the hippocampus and cortex of APP/PS1 double transgenic mice using transmission electron microscopy.
  
  
  RESULTS
  Damage to mitochondrial morphology in the hippocampus and cortex of APP/PS1 double transgenic mice was found, including swelling and cavitations. Our analysis showed no statistical differences in the expression of HUMMR between APP/PS1 double transgenic mice and WT littermates (p > 0.05). These results showed that there was no association between HUMMR and mitochondrial dysfunction in APP/PS1 transgenic mice.
  
  
  CONCLUSIONS
  These results indicate that HUMMR does not play a key role in mitochondrial dysfunction in the APP/PS1 double transgenic AD mouse.
authors.affiliation: Department of Geriatrics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Zou
authors.forename: Yu
authors.initials: Y
authors.lastname: Li
authors.forename: Weihua
authors.initials: W
authors.lastname: Yu
authors.forename: Yingshi
authors.initials: Y
authors.lastname: Du
authors.forename: Rui
authors.initials: R
authors.lastname: Shi
authors.forename: Man
authors.initials: M
authors.lastname: Zhang
authors.forename: Jingxi
authors.initials: J
authors.lastname: Duan
authors.forename: Yongtao
authors.initials: Y
authors.lastname: Deng
authors.forename: Qi
authors.initials: Q
authors.lastname: Tu
authors.forename: Rong
authors.initials: R
authors.lastname: Dai
authors.forename: Yang
authors.initials: Y
authors.lastname: Lü
mesh_terms: D000544:Alzheimer Disease / Q000235:genetics* / Q000523:psychology; D016564:Amyloid beta-Protein Precursor / Q000235:genetics* / Q000502:physiology*; D000818:Animals; D015153:Blotting, Western; D002540:Cerebral Cortex / Q000473:pathology / Q000648:ultrastructure; D005091:Exons / Q000235:genetics; D005136:Eye Proteins; D005260:Female; D006624:Hippocampus / Q000473:pathology / Q000648:ultrastructure; D006801:Humans; D008297:Male; D008565:Membrane Proteins / Q000235:genetics* / Q000502:physiology*; D051379:Mice; D008822:Mice, Transgenic; D008854:Microscopy, Electron; D008928:Mitochondria / Q000502:physiology / Q000648:ultrastructure; D024101:Mitochondrial Proteins; D053764:Presenilin-1 / Q000235:genetics* / Q000502:physiology*; D060888:Real-Time Polymerase Chain Reaction; D019076:Transgenes
chemical_list: D016564:Amyloid beta-Protein Precursor; D005136:Eye Proteins; C509731:MGARP protein, mouse; D008565:Membrane Proteins; D024101:Mitochondrial Proteins; D053764:Presenilin-1