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Sandro Alves

Researcher at Université Paris-Saclay

Publications -  32
Citations -  6856

Sandro Alves is an academic researcher from Université Paris-Saclay. The author has contributed to research in topics: Neurodegeneration & Autophagy. The author has an hindex of 19, co-authored 32 publications receiving 6166 citations. Previous affiliations of Sandro Alves include University of Coimbra & Allen Institute for Brain Science.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Sustained effects of nonallele-specific Huntingtin silencing†

Valérie Drouet, +18 more
- 01 Mar 2009 - 
TL;DR: This work has shown that RNA interference represents a promising approach for the treatment of autosomal dominant disorders, but whether an allele‐specific silencing of mutant htt or a nonallele‐ specific silencing should be considered has not been addressed.
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Overexpression of the autophagic beclin-1 protein clears mutant ataxin-3 and alleviates Machado-Joseph disease.

Isabel Nascimento-Ferreira, +15 more
- 01 May 2011 - 
TL;DR: It is demonstrated that autophagy is a key degradation pathway, with beclin-1 playing a significant role in alleviating Machado-Joseph disease pathogenesis.
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Allele-specific RNA silencing of mutant ataxin-3 mediates neuroprotection in a rat model of Machado-Joseph disease.

Sandro Alves, +16 more
- 08 Oct 2008 - 
TL;DR: Data demonstrate that RNAi has potential for use in MJD treatment and constitute the first proof-of-principle for allele-specific silencing in the central nervous system.
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CYP46A1, the rate-limiting enzyme for cholesterol degradation, is neuroprotective in Huntington’s disease

Lydie Boussicault, +17 more
- 29 Jan 2016 - 
TL;DR: Restoration of CYP46A1 re-establishes normal cholesterol levels and is neuroprotective, suggesting that targeting cholesterol degradation may have therapeutic potential.