Blocking GluR2-GAPDH ameliorates experimental autoimmune encephalomyelitis.

ABSTRACT:

Objective

Multiple sclerosis (MS) is the most common disabling neurological disease of young adults. The pathophysiological mechanism of MS remains largely unknown and no cure is available. Current clinical treatments for MS modulate the immune system, with the rationale that autoimmunity is at the core of MS pathophysiology.

Methods

Experimental autoimmune encephalitis (EAE) was induced in mice with MOG35-55 and clinical scoring was performed to monitor signs of paralysis. EAE mice were injected intraperitoneally with TAT-fusion peptides daily from day 10 until day 30 after immunization, and their effects were measured at day 17 or day 30.

Results

We report a novel target for the development of MS therapy, which aimed at blocking glutamate-mediated neurotoxicity thro

SUBMITTER: Zhai D 

PROVIDER: S-EPMC4402084 | biostudies-literature | 2015 Apr

REPOSITORIES: biostudies-literature