Exosomes (EXOs), minute membranous structures originating from diverse biological sources, have recently seized the attention of researchers due to their theranostic potential for neurological diseases. Released actively by various cells, including stem cells, adipose tissue, and immune cells, EXOs wield substantial regulatory influence over the intricate landscape of neurological complications, exhibiting both positive and negative modulatory effects. In AD, EXOs play a pivotal role in disseminating and breaking down amyloid-β protein. Moreover, EXOs derived from mesenchymal stem cells showcase a remarkable capacity to mitigate pro-inflammatory phenotypes by regulating miRNAs in neurodegenerative diseases. These vesicles possess the unique ability to traverse the blood-brain barrier, governing the aggregation of mutant huntingtin protein. Understanding the exosomal functions within the CNS holds significant promise for enhancing treatment efficacy in neurological diseases. This review intricately examines the regulatory mechanisms involving EXOs in neurological disease development, highlighting therapeutic prospects and exploring their utility in exosome-based nanomedicine for various neurological complications. Additionally, the review delves into the challenges associated with drug delivery to the brain, emphasizing the complexities inherent in this critical aspect of neurotherapeutics.

Multiple sclerosis (MS) is a complex autoimmune disease characterised by inflammation, demyelination, and neurodegeneration within the central nervous system (CNS). While the exact causes remain unclear, recent research highlights the significant role of epigenetic modifications and mitochondrial dysfunction in the disease’s onset and progression. Epigenetic alterations, such as DNA methylation, histone modification, and microRNA regulation, influence gene expression without altering the DNA sequence, leading to immune dysregulation and inflammation. Similarly, mitochondrial dysfunction, marked by impaired oxidative phosphorylation, reduced adenosine triphosphate (ATP) production, and increased reactive oxygen species (ROS), contributes to neurodegeneration and impaired remyelination in MS. The growing interest in targeting these two interconnected mechanisms has opened new avenues for MS treatment. Herbal drugs, known for their multi-targeted effects, have shown potential in modulating epigenetic markers and enhancing mitochondrial function. Compounds such as resveratrol, curcumin, epigallocatechin-3-gallate (EGCG), quercetin, and omega-3 fatty acids demonstrate potential in regulating DNA methylation, histone deacetylation, and mitochondrial biogenesis. These natural agents offer dual-action therapies by reducing oxidative stress and inflammation while promoting neuronal survival and remyelination. This review explores the therapeutic potential of herbal drugs targeting epigenetic and mitochondrial pathways in MS, evaluating their mechanisms of action and highlighting their promise as novel therapeutic agents. While initial findings are encouraging, further research and clinical trials are required to validate the efficacy of these herbal treatments and fully understand their potential in slowing disease progression and improving patient outcomes in MS. Such exploration could pave the way for safer, multi-targeted therapies, offering new hope in the management of MS and other neurodegenerative diseases.