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eISSN: 1509-572x
ISSN: 1641-4640
Folia Neuropathologica
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abstract:
Original paper

NAD+ attenuates central nervous system demyelination in experimental autoimmune encephalomyelitis mice

Bin Zheng
1
,
Jianhua Ma
2
,
Xiao Deng
3
,
Jiangang Pan
4
,
Feng Liao
4

  1. Department of Neurosurgery, The Second Affiliated Hospital of Shandong First Medical University, Taian, Shandong Province, China
  2. Department of Vascular Surgery, People’s Hospital of Feicheng, Feicheng City, Taian, Shandong Province, China
  3. Department of Rehabilitation Medicine, The Second Affiliated Hospital of Guangdong Medical University, Xiashan District, Zhanjiang, Guangdong Province, China
  4. Department of Neurology, Affiliated Hospital of Guangdong Medical University, Xiashan District, Zhanjiang, Guangdong Province, China
Folia Neuropathol 2025; 63
Online publish date: 2025/02/11
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Nicotinamide adenine dinucleotide (NAD+) supplementation attenuates demyelination in the experimental autoimmune encephalomyelitis (EAE) model. The aim of the study was to confirm the therapeutic effect of NAD+ on the EAE model and investigate its protective mechanism. Mice were divided into 3 groups: EAE, EAE + NAD+, and Control (Ctrl). EAE and EAE + NAD+ groups were induced with myelin oligodendrocyte glycoprotein (MOG) to initiate the demyelination process. The EAE + NAD+ group received an NAD+ injection at a dosage of 250 mg/kg/day. Clinical, neuroinflammation, and neurodemyelination scores were monitored. At the peak of onset, animals were euthanized, and mRNA expression level in the spinal cord was tested. NAD+ supplementation promoted the conversion of regulatory T cells (Tregs) into T helper 17 (Th17) cells with increased concentrations of NAD+. NAD+ alleviated neuroinflammation, attenuated central nervous system (CNS) demyelination, and improved the disease score of EAE mice. NAD+ promoted expression of the cytokine interleukin 17A (IL-17A).
keywords:

experimental autoimmune encephalomyelitis, IL-17A, multiple sclerosis, NAD+, neuroinflammation, Th17 cell, Treg cell

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