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Genetically modified immune cells, especially CAR‐T cells, have captured the attention of scientists over the past 10 years. In the fight against cancer, these cells have a special place. Treatment for hematological cancers, autoimmune disorders, and cancers must include CAR‐T cell therapy. Determining the therapeutic targets, side effects, and use of CAR‐T cells in neurological disorders, including cancer and neurodegenerative diseases, is the goal of this study. Due to advancements in genetic engineering, CAR‐T cells have become crucial in treating some neurological disorders. CAR‐T cells have demonstrated a positive role in treating neurological cancers like Glioblastoma and Neuroblastoma due to their ability to cross the blood–brain barrier and use diverse targets. However, CAR‐T cell therapy for MS diseases is being researched and could be a potential treatment option. This study aimed to access the most recent studies and scientific articles in the field of CAR‐T cells in neurological diseases and/or disorders.

Background Photobiomodulation therapy (PBM), due to its anti-inflammatory, analgesic effects, and most importantly as a non-invasive procedure, has currently gained a special setting in pain relief and the treatment of Spinal cord injuries (SCI). However, the mechanism of action of the PBM is not yet completely understood. Methods In this study, SCI is induced by an aneurysm clip. Adult male rats were divided into 4 groups: Control, SCI, SCI + PBMT 90 seconds, and SCI + PBMT 117 seconds. After 7 weeks, hyperalgesia, allodynia, and functional recovery were assessed. Fibroblasts were counted after H&E staining. The expression of HDAC2, DNMT3a, GAD65, and GFAP after 4 weeks of daily PBMT (90 and 117 s) was probed by western blotting. Results Both PBMTs (90 & 117 seconds) significantly improved the pain and ability to move and fibroblast invasion was reduced. SCI + PBMT 90s, increased GAD65, HDAC2, and DNMT3a expression. However,PBMT 117s decreased GFAP, HDAC2, and DNMT3a. Conclusion PBMT 90 and 117 s improved the pain, and functional recovery equally. Yet, the mechanism of action appears to change with different durations of radiation.

Photobiomodulation therapy (PBMT) is converted to the most common analgesic treatment before the whole mechanism is yet to be discovered. This study for the first time was designed to investigate alternations of epigenetic factors after pain and PBMT. The CCI model was chosen to induce pain. Pain evaluation tests including plantar, acetone, von Frey, and pinch were done weekly. Then spinal cord tissue was isolated for evaluating mRNA expression of DNMT3a, HDAC1, and NRSF using RT‐qPCR method, and protein expression factors of HDAC2 and DNMT3a using western blotting. GAD65 and TGF‐β proteins were assessed by the IHC method. PBMT increased the pain threshold up to the point where it roughly met the pain threshold of the control group. After three weeks of treatment, both PBMT protocols demonstrated a reduction in allodynia and hyperalgesia. While some molecules, such as TGF‐β and Gad65, increased following PBMT, we observed no inhibition of NRSF, HDAC1, and DNMT3a expression despite implementing two different protocols.