Study type: In vivo/preclinical · Status: Verified against declared source

VPAC1 receptor (Vipr1)-deficient mice exhibit ameliorated experimental autoimmune encephalomyelitis, with specific deficits in the effector stage.

Journal of neuroinflammation · 2016

Study scale: EAE is a multistep pathology in which two phases have been characterized: the immunization and the effector phase.

Abstract only: Open source record

Product or molecular entity relationships

VIP: Exact entity relationship. Legacy citation custody associates this source with the catalog record; no product-relevance conclusion is implied.

Plain-language verified summary

Question

We recently began to examine the relevance of the endogenous neuropeptides and the role of receptor subtypes by gene deletion in the murine model of experimental autoimmune encephalomyelitis (EAE), a widely used model for MS [31].

Methods

The online version of this article (doi:10.1186/s12974-016-0626-3) contains supplementary material, which is available to authorized users.

Scale or participants

EAE is a multistep pathology in which two phases have been characterized: the immunization and the effector phase.

Key findings

MOG35–55-induced EAE was ameliorated in VPAC1 KO mice compared to WT mice.

Limitations and uncertainty

Vasoactive intestinal peptide (VIP) and pituitary adenylyl cyclase-activating polypeptide (PACAP) are two highly homologous neuropeptides.

Verified against declared source. Verification is limited to the declared source and review scope. It does not mean independent replication or establish efficacy, safety, or suitability.