Author Correction: Transneuronal propagation of mutant huntingtin contributes to non-cell autonomous pathology in neurons.

In the version of this article initially published, the catalog numbers for BoNT A and B were given in the Methods section as T0195 and T5644; the correct numbers are B8776 and B6403. The error has been corrected in the HTML and PDF versions of the article.

Building a global surgery initiative through evaluation, collaboration, and training: the Massachusetts General Hospital experience.

Objective: The Massachusetts General Hospital (MGH) Department of Surgery established the Global Surgery Initiative (GSI) in 2013 to transform volunteer and mission-based global surgery efforts into an educational experience in surgical systems strengthening. The objective of this newly conceived mission is not only to perform advanced surgery but also to train surgeons beyond MGH through international partnerships across disciplines. At its inception, a clear pathway to achieve this was not established, and we sought to identify steps that were critical to realizing our mission statement.

Transneuronal propagation of mutant huntingtin contributes to non-cell autonomous pathology in neurons.

In Huntington's disease (HD), whether transneuronal spreading of mutant huntingtin (mHTT) occurs and its contribution to non-cell autonomous damage in brain networks is largely unknown. We found mHTT spreading in three different neural network models: human neurons integrated in the neural network of organotypic brain slices of HD mouse model, an ex vivo corticostriatal slice model and the corticostriatal pathway in vivo. Transneuronal propagation of mHTT was blocked by two different botulinum neurotoxins, each known for specifically inactivating a single critical component of the synaptic vesicle fusion machinery.