Stimulation of autophagy by rapamycin protects neurons from remote degeneration after acute focal brain damage

Maria Teresa Viscomi, Marcello D'Amelio, Virve Cavallucci, Laura Latini, Elisa Bisicchia, Francesca Nazio, Francesca Fanelli, Mauro Maccarrone, Sandra Moreno, Francesco Cecconi, Marco Molinari

Research output: Contribution to journalArticlepeer-review


Autophagy is the evolutionarily conserved degradation and recycling of cellular constituents. In mammals, autophagy is implicated in the pathogenesis of many neurodegenerative diseases. However, its involvement in acute brain damage is unknown. This study addresses the function of autophagy in neurodegeneration that has been induced by acute focal cerebellar lesions. We provide morphological, ultrastructural, and biochemical evidence that lesions in a cerebellar hemisphere activate autophagy in axotomized precerebellar neurons. Through time course analyses of the apoptotic cascade, we determined mitochondrial dysfunction to be the early trigger of degeneration. Further, the stimulation of autophagy by rapamycin and the employment of mice with impaired autophagic responses allowed us to demonstrate that autophagy protects from damage promoting functional recovery. These findings have therapeutic significance, demonstrating the potential of pro-autophagy treatments for acute brain pathologies, such as stroke and brain trauma.

Original languageEnglish
Issue number2
Publication statusPublished - Feb 2012


  • Acute brain damage
  • Neurodegeneration
  • Neuronal death
  • Neuroprotection
  • Rapamycin

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology


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