Multiple sclerosis is a demyelinating disease of the central nervous system characterized by the loss of the myelin sheath-the nonconductive membrane surrounding neuronal axons. Demyelination interrupts neuronal transmission, which can impair neurological pathways and present a variety of neurological deficits. Prolonged demyelination can damage neuronal axons resulting in irreversible neuronal damage. Efforts have been made to identify agents that can promote remyelination. However, the assessment of remyelination that new therapies promote can be challenging. The method described in this chapter addresses this challenge by using isobaric C13-histidine as a tag for monitoring its incorporation into myelin proteins and thus monitoring the remyelination process.
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http://dx.doi.org/10.1007/978-1-0716-2699-3_17 | DOI Listing |
J Neurol
January 2025
Department of Neurology, University Hospital Frankfurt, Frankfurt Am Main, Germany.
Background: BDNF has increasingly gained attention as a key molecule controlling remyelination with a prominent role in neuroplasticity and neuroprotection. Still, it remains unclear how BDNF relates to clinicoradiological characteristics particularly at the early stage of the disease where precise prognosis for the further MS course is crucial.
Methods: BDNF, NfL and GFAP concentrations in serum and CSF were assessed in 106 treatment naïve patients with MS (pwMS) as well as 73 patients with other inflammatory/non-inflammatory neurological or somatoform disorders using a single molecule array HD-1 analyser.
Adv Sci (Weinh)
January 2025
Department of Orthopedics, The First Affiliated Hospital, Jinan University, Guangzhou, 510632, China.
Spinal cord injury (SCI) impairs the central nervous system and induces the myelin-sheath-deterioration because of reactive oxygen species (ROS), further hindering the recovery of function. Herein, the simultaneously emergency treatment and dynamic luminescence severity assessment (SETLSA) strategy is designed for SCI based on cerium (Ce)-doped upconversion antioxidant nanoenzymes (Ce@UCNP-BCH). Ce@UCNP-BCH can not only efficiently eliminate the SCI localized ROS, but dynamically monitor the oxidative state in the SCI repair process using a ratiometric luminescence signal.
View Article and Find Full Text PDFBackground: As a key inflammatory factor, the nucleotide-binding oligomerization domain (NOD)-like receptor protein 3 (NLRP3) inflammasome plays a crucial role in neuroinflammation and the progression of neurodegenerative diseases. Dysregulation of NLRP3 signaling can trigger various inflammatory responses in the brain, contributing to the development of neurodegenerative diseases such as ischemic stroke, vascular dementia (VaD), Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS). Therefore, the NLRP3 signaling pathway is a promising therapeutic target for the treatment of neurodegenerative diseases, including VaD.
View Article and Find Full Text PDFTheranostics
January 2025
State Key Laboratory of Medical Neurobiology, MOE Frontiers Center for Brain Science, and Institutes of Brain Science, Fudan University, Shanghai, China.
J Ethnopharmacol
December 2024
School of Traditional Chinese Medicine, Capital Medical University, Beijing, China. Electronic address:
Ethnopharmacological Relevance: The Bu Shen Yi Sui capsule (BSYS), a modified version of the classical Chinese medicine formula Liu Wei Di Huang pill, has demonstrated therapeutic efficacy in the treatment of multiple sclerosis (MS). Nevertheless, the precise mechanism through which BSYS facilitates remyelination remains to be elucidated.
Aim Of The Study: This research investigates the role and potential mechanisms of BSYS-modified exosomes (exos) derived from bone marrow mesenchymal stem cells (BMSCs) in promoting remyelination in a cuprizone (CPZ)-induced demyelination model in mice.
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