Selective autophagy as a potential therapeutic target for neurodegenerative disorders

Aurora Scrivo, Mathieu Bourdenx, Olatz Pampliega, Ana Maria Cuervo

Research output: Contribution to journalReview articlepeer-review

197 Scopus citations


Cells rely on surveillance systems such as autophagy to handle protein alterations and organelle damage. Dysfunctional autophagy, an evolutionarily conserved cellular mechanism for degradation of intracellular components in lysosomes, frequently leads to neurodegeneration. The neuroprotective effect of autophagy stems from its ability to eliminate pathogenic forms of proteins such as α-synuclein or tau. However, the same pathogenic proteins often affect different types and steps of the autophagic process. Furthermore, genetic studies have shown that some proteins related to neurodegeneration, such as huntingtin, participate in autophagy as one of their physiological functions. This complex interplay between autophagy and neurodegeneration suggests that targeting autophagy as a whole might have limited applicability in neurodegenerative diseases, and that future efforts should focus instead on targeting specific types and steps of the autophagic process. This change of strategy in the modulation of autophagy might hold promise for future disease-modifying therapies for patients with neurodegenerative disorders.

Original languageEnglish (US)
Pages (from-to)802-815
Number of pages14
JournalThe Lancet Neurology
Issue number9
StatePublished - Sep 2018

ASJC Scopus subject areas

  • Clinical Neurology


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