Mitochondrial Dysfunction in Alzheimer’s Disease and Progress in Mitochondria-Targeted Therapeutics

Padraig J. Flannery, Eugenia Trushina

Research output: Contribution to journalReview articlepeer-review

6 Scopus citations


Purpose of Review: Mitochondria are essential for facilitating energy homeostasis under ever-changing environmental conditions. Mitochondrial dysfunction has been suggested to either play a primary role in the development of multiple human diseases and/or significantly contribute to disease progression. Here, we review recent findings on mitochondrial dysfunction in Alzheimer’s disease (AD) and strategies for the development of mitochondria-targeted therapies. Recent Findings: Multiple mechanisms essential for proper mitochondrial functioning including biogenesis and turnover, fission/fusion, trafficking, and bioenergetics are affected in AD. Few therapeutic strategies were developed to address these problems. Summary: While a conclusive statement on the causative role of mitochondrial dysfunction in AD remains elusive, the available evidence suggests that improving mitochondrial function via pharmacological and/or non-pharmacological interventions could delay the onset and slow the progression of AD. Further research and outcomes of ongoing clinical trials should extend our understanding and help to validate conclusions regarding causation.

Original languageEnglish (US)
Pages (from-to)88-102
Number of pages15
JournalCurrent Behavioral Neuroscience Reports
Issue number3
StatePublished - Sep 15 2019


  • Alzheimer’s disease
  • Mitochondria
  • Mitochondria-targeted therapeutics

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health
  • Behavioral Neuroscience


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