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D-SERINE REFLECTS INTRATHECAL INFLAMMATION IN MULTIPLE SCLEROSIS AND COUNTERACTS MOTOR IMPAIRMENT IN A MURINE MODEL
Alessandro Usielloand 21 co-authors
Università degli Studi della Campania Luigi Vanvitelli
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS03-08AM-002
Presentation
Date TBA
Board: PS03-08AM-002
Event Information
Poster Board
PS03-08AM-002
Poster
View posterAbstract
Multiple sclerosis (MS) is characterized by chronic inflammatory demyelination involving interplay between the central nervous and immune systems. Neuroinflammation reorganizes cellular metabolism, requiring L-serine for membrane and nucleotide synthesis, while also disturbing glutamatergic neurotransmission via D-serine. However, significance of serine metabolism in MS remains unexplored. Here we show that serine chiral homeostasis is disrupted in MS and endogenous D-serine prevents motor deficits caused by inflammatory demyelination. In a large cohort study, patients with MS exhibited elevated D-serine levels and the D-/total serine ratio in cerebrospinal fluid at diagnosis. This deviation toward D-serine accords with emergence of intrathecal inflammatory marker oligoclonal bands, and correlates negatively with proinflammatory cytokines. An in vivo animal model of MS, genetically engineered to exhibit distinct metabolic states of D-serine, revealed that endogenous D-serine synthesis mitigates motor deficits and suppresses proinflammatory and vascular endothelial signaling. Moreover, pre-symptomatic oral supplementation with D-serine, but not L-serine, enhances extracellular matrix production, preserves blood brain barrier integrity, attenuates demyelination, and improves motor function. Contrary to the recognized neurotoxic nature of D-serine, our findings identify a protective role of D-serine in limiting neuroinflammation, highlighting D-serine metabolism as a potential therapeutic target in MS.
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