Impacts of H2O2, SARM1 inhibition, and high NAm concentrations on Huntington's disease laser-induced degeneration

被引：0
|
作者：
Barber, Sophia [1 ,2 ]
Gomez-Godinez, Veronica [1 ,3 ]
Young, Joy [1 ]
Wei, Abigail [1 ]
Chen, Sarah [1 ]
Snissarenko, Anna [2 ]
Chan, Sze Sze [2 ]
Wu, Chengbiao [1 ,2 ]
Shi, Linda [1 ,3 ]
机构：
[1] Univ Calif San Diego, Inst Engn Med, La Jolla, CA USA
[2] Univ Calif San Diego, Dept Neurosci, La Jolla, CA USA
[3] Univ Calif San Diego, Inst Engn Med, La Jolla, CA 92093 USA
来源：
JOURNAL OF BIOPHOTONICS | 2024年 / 17卷 / 03期
关键词：
axonal damage; cell morphology; dorsal root ganglion cells; Huntington's disease; laser cutting; neurons; NEURONAL INTRANUCLEAR INCLUSIONS; PROJECTION NEURONS; AXONAL-TRANSPORT; GENE; HD; REPEAT;
D O I：
10.1002/jbio.202300370
中图分类号：
Q5 [生物化学];
学科分类号：
071010 ; 081704 ;
摘要：
Axonal degeneration is a key component of neurodegenerative diseases such as Huntington's disease (HD), Alzheimer's disease, and amyotrophic lateral sclerosis. Nicotinamide, an NAD+ precursor, has long since been implicated in axonal protection and reduction of degeneration. However, studies on nicotinamide (NAm) supplementation in humans indicate that NAm has no protective effect. Sterile alpha and toll/interleukin receptor motif-containing protein 1 (SARM1) regulates several cell responses to axonal damage and has been implicated in promoting neuronal degeneration. SARM1 inhibition seems to result in protection from neuronal degeneration while hydrogen peroxide has been implicated in oxidative stress and axonal degeneration. The effects of laser-induced axonal damage in wild-type and HD dorsal root ganglion cells treated with NAm, hydrogen peroxide (H2O2), and SARM1 inhibitor DSRM-3716 were investigated and the cell body width, axon width, axonal strength, and axon shrinkage post laser-induced injury were measured.
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页数：14
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