Review highlights the connection between neuroinflammation in multiple sclerosis and the microbiome, suggesting implications for treatment.
A significant amount of the health care burden in contemporary society is attributed to neurodegenerative diseases (NDs). Because of longer lifespans and changes in the world's population, the prevalence of these diseases will rise even more in the future decades. The primary cause of NDs is the progressive degeneration of neurones, which leads to dementia, motor impairments, and other associated functional impairments. Numerous illnesses, including Huntington's disease (HD), Parkinson's disease (PD), Alzheimer's disease (AD), and Amyotrophic Lateral Sclerosis (ALS), are brought on by these alterations. Neurone death, dendritic loss, and demyelination are general pathophysiological indicators. Furthermore, a number of molecular processes have been postulated to explain the pathophysiology of these disorders, while the precise reason is still unknown. Neuroinflammation and oxidative stress are the most prevalent. With regard to neuroinflammation, we attempt to draw attention to a neglected factor in the aetiology of multiple sclerosis in this review. Protein domains found in a number of bacteria imitate the cellular proteins found in the nervous system. As a result, even when the viruses are removed from the body, the immune system never stops functioning. Native proteins are nonetheless regarded as alien proteins, and the cells die as a result of subsequent immune cell activation and communication. As a result, we have compiled the research supporting this theory to link it to other chemical pathways in NDs.
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Nayana et al. (2025) studied this question.
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