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Related Experiment Video

Updated: Feb 27, 2026

Experimental Demyelination and Remyelination of Murine Spinal Cord by Focal Injection of Lysolecithin

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Nicotinamide Administration Improves Remyelination after Stroke.

Congxiao Wang¹, Yi Zhang¹, Jie Ding¹

¹Jiangsu Key Laboratory of Molecular and Functional Imaging, Department of Radiology, Zhongda Hospital, Medical School of Southeast University, Nanjing 210009, China.

Neural Plasticity

|June 29, 2017

Summary

Nicotinamide treatment improved brain repair after stroke by enhancing remyelination. This occurred through increased NAD+, brain-derived neurotrophic factor (BDNF), and the TrkB pathway, leading to better functional recovery.

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Area of Science:

Neuroscience
Biochemistry
Regenerative Medicine

Background:

Stroke is a major cause of disability and death.
Effective treatments for stroke recovery, particularly promoting neural repair, are urgently needed.

Purpose of the Study:

To investigate the potential of nicotinamide to enhance remyelination post-stroke.
To elucidate the molecular mechanisms underlying nicotinamide's effects on stroke recovery.

Main Methods:

Adult mice received nicotinamide or saline after middle cerebral artery occlusion.
Inhibitors of NAMPT (FK866) and TrkB (ANA-12) were used to probe the mechanism.
Functional recovery, MRI, and histological assessments were performed.

Main Results:

Nicotinamide reduced infarct size and improved white matter integrity (FA).
Treatment increased levels of NAD+, BDNF, and remyelination markers.
FK866 blocked nicotinamide's effects, while ANA-12 impaired recovery.

Conclusions:

Nicotinamide administration promotes remyelination after stroke.
The mechanism involves the NAD+/BDNF/TrkB signaling pathway.
This suggests a potential therapeutic strategy for stroke recovery.