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Advanced Neurology Multiple sclerosis: Immunopathogenesis

suggesting their involvement in the progression of MS . these epitopes is related to CNS antigens remains an open
[90]
Numerous studies have shown that individuals who question .
[94]
develop ON as the first clinical symptom of MS have a Studies are still underway to better understand how
lower degree of disability, whereas MS first appears in inflammatory demyelination processes in the optic nerve
other neurological structures. Serum adiponectin, leptin, leads to loss of retinal ganglion cells in the retinal layer of
and resistin concentration were remarkably lower in the eye. Research on the early molecules of the complement
patients with ON as the first symptom compared to ON pathway, C1q and C3, has led to the hypothesis that
negative as first symptom (adiponectin P = 0.004, leptin deviation in complement expression by astroglia leads
P = 0.013, resistin P = 0.006). Curiously, healthy control to neurotoxicity . In addition, recent studies have
[95]
subjects and patients with ON as their first clinical episode shown that C3 is primarily expressed in neurotoxic
had similar adiponectin, leptin, and resistin levels .
[90]
astrocytes [96,97] . Immunohistochemical staining has
Research was conducted to evaluate the changes in identified a neurotoxic subtype of optic nerve astrocytes
brain structural volume. In MS active individuals, the that express greater amounts of complement component 3
loss of ganglion cell volume and inner plexiform layer (C3) . Early complement pathway molecules such as C1q
[98]
as well as total brain mass was two times greater and and C3 may have the ability to mediate neurodegenerative
five times faster in thalamic regions than in MS-stable processes in MS . Yes-associated protein (YAP) has been
[21]
patients during the first 2 years after the onset of MS, implicated in the mechanism of neuroinflammation and
although these strong contrasts decreased 5 years after may upregulate the expression of transforming growth
the onset of MS [91] . With the aid of optical coherence factor beta (TGFβ) to prevent inflammatory responses,
tomography, retinal damage was found in association demyelination, and retinal ganglion cell death in ON .
[99]
with neuroinflammation, particularly in acute ON, and Based on research and also clinical practice, not only
similar changes have been observed in patients with MS. the pathogenesis of ON, but also the clinical features are
Under the premise of the association of retinal atrophy linked with MS. Therefore, further investigation may
with brain atrophy, researchers used MS model to lead to the discovery of markers for detecting early-stage
study acute and chronic in vivo molecules in the retina demyelination, which is instrumental for predicting
during acute and chronic ON by employing the Raman disease development and if necessary, initiating early
spectroscope. Ten different molecules that correlate treatment.
with cellular energy and axon biology were selected.
It was found that age was the major determinant of 7. Conclusions
the concentration changes of some molecules. The In Western countries, MS is the leading cause of neurological
most striking alteration was the change in metabolites disability and typically occurs more frequently in women
related to mitochondria and energy supply (NADH and than in men. The etiopathogenesis of MS is a complex
FAD) [92] .
and multistage process encompassing inflammation,
One study examined the relationship between visual demyelination, and neurodegeneration, in which genetic
evoked potentials and thiol-disulfide homeostasis, a and environmental factors are at play. The smouldering MS
measure of redox imbalance. The study provided evidence hypothesis may help explain disease progression during
that during an episode of ON in MS, there was a delay in the remission phase. Early diagnosis of the disease could
nerve signal transmission from the retina to the visual be realized using biological markers for disease detection,
cortices, known as P100 wave latency, while the thiol- but the search for specific and accurate diagnostic markers
disulfide balance shifted in favor of disulfides . is currently in progress. Optic neuritis is an important
[93]
Since MS is mainly triggered by autoimmune manifestation of MS, which is part of the criteria for
reactions against the CNS, CSF examination should be early diagnosis of demyelinating disease. In conclusion,
the priority in the search for biomarkers. A study has establishing a more comprehensive set of diagnostic
shown that the epitopes of A and B likely mimic the high- criteria for MS is a prerequisite for earlier detection and
affinity antigenic epitopes of cytomegalovirus and EBV, diagnosis of MS, which is crucial for earlier prescription
corroborating these epitopes as potent candidates for of treatments to improve the patient’s condition and halt
serological biomarkers . The high-antigenic epitopes disease progression.
[94]
of glycoprotein B cytomegalovirus and VCA p18 EBV Acknowledgments
suggest their role in the pathogenesis of MS, although
how the humoral response of the immune system against None.

Volume 2 Issue 3 (2023) 9 https://doi.org/10.36922/an.1319