Paradigms in multiple sclerosis: time for a change, time for a unifying concept.

Area of Science:

• Neuroimmunology
• Developmental Neuroscience
• Biochemistry

Background:

• Multiple sclerosis (MS) is traditionally viewed as an autoimmune disease.
• Emerging theories propose MS as a neurocristopathy, stemming from neural crest development issues.
• Several factors, including hygiene, human endogenous retroviruses (HERVs), vitamin D, and immune responses, are implicated in MS etiology.

Purpose of the Study:

• To explore a unifying concept for MS pathogenesis, integrating neurocristopathy and redox dysregulation.
• To investigate the role of melanin-like pigments in nerve tissue in MS.
• To explain the spatial and temporal characteristics of MS based on proposed mechanisms.

Main Methods:

• Review and synthesis of existing literature on MS etiology, neurocristopathy, and melanin biochemistry.
• Analysis of proposed mechanisms involving redox regulation, oxidative stress, and pigment function.
• Consideration of adaptive neuronal changes and external factors like UV light and stress.

Main Results:

• A novel hypothesis suggests MS pathogenesis involves disturbed redox regulation in melanin-like pigment biosynthesis, potentially linked to altered vitamin D metabolism and HERV expression.
• Pathological melanin pigments may explain MS symptoms, including responses to light and vitamin D, via oscillating oxidative processes.
• Increased mitochondria in demyelinated neurons and stress contribute to MS pathology.

Conclusions:

• The proposed unifying concept integrates neurocristopathy, melanin pigment redox dysregulation, and neuronal adaptation to explain MS.
• This framework offers new perspectives for MS prevention, diagnosis, and therapy.
• Early childhood vaccination against Epstein-Barr virus is suggested as a potential preventive measure.