Interventions that improve body and brain bioenergetics for parkinson's disease risk reduction and therapy

Mark P. Mattson

Research output: Contribution to journalArticlepeer-review

36 Scopus citations


Studies of Parkinson's disease (PD) patients, animal models and pathogenic actions of genetic mutations that cause familial PD have established that neuronal bioenergetics are compromised with brainstem and midbrain monoaminergic neurons being particularly vulnerable. Peripheral insulin resistance and diabetes in midlife may increase the risk of PD, and diet and lifestyle changes that increase insulin sensitivity (exercise and intermittent energy restriction) can counteract neurodegenerative processes and improve functional outcome in animal models. Insulin sensitizing glucagon-like peptide 1 (GLP-1) analogs are beneficial in animal models of PD, and the results of an initial clinical trial in PD patients are promising. In addition to improving peripheral and brain energy metabolism, exercise, intermittent energy restriction and GLP-1 analogs may bolster neuronal adaptive stress response pathways that enhance neurotrophic signaling, DNA repair, proteostasis and mitochondrial biogenesis.

Original languageEnglish (US)
Pages (from-to)1-13
Number of pages13
JournalJournal of Parkinson's Disease
Issue number1
StatePublished - 2014


  • Autonomic nervous system
  • autophagy
  • brainstem
  • exercise
  • GLP-1
  • insulin
  • intermittent fasting
  • mitochondrial biogenesis
  • synuclein

ASJC Scopus subject areas

  • Clinical Neurology
  • Cellular and Molecular Neuroscience


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