Alterations in mitochondrial number and function in Alzheimer’s disease fibroblasts

Nora E. Gray, Joseph F. Quinn

Research output: Contribution to journalArticle

12 Scopus citations

Abstract

Mitochondrial dysfunction is observed in brains of Alzheimer’s Disease patients as well as many rodent model systems including those modeling mutations in preseinilin 1 (PSEN1). The aim of our study was to characterize mitochondrial function and number in fibroblasts from AD patients with PSEN1 mutations. We used biochemical assays, metabolic profiling and fluorescent labeling to assess mitochondrial number and function in fibroblasts from three AD patients compared to fibroblasts from three controls. The mutant AD fibroblasts had increased Aβ42 relative to controls along with reduction in ATP, basal and maximal mitochondrial respiration as well as impaired spare mitochondrial respiratory capacity. Fluorescent staining and expression of genes encoding electron transport chain enzymes showed diminished mitochondrial content in the AD fibroblasts. This study demonstrates that mitochondrial dysfunction is observable in AD fibroblasts and provides evidence that this model system could be useful as a tool to screen disease-modifying compounds.

Original languageEnglish (US)
Pages (from-to)1275-1278
Number of pages4
JournalMetabolic brain disease
Volume30
Issue number5
DOIs
StatePublished - Oct 10 2015

Keywords

  • Alzheimer’s disease
  • Mitochondrial dysfunction
  • β-amyloid

ASJC Scopus subject areas

  • Biochemistry
  • Clinical Neurology
  • Cellular and Molecular Neuroscience

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