No abstract

Multiple sclerosis (MS) is an autoimmune demyelinating disease of the central nervous system and the most common neurological disease in young adults, affecting more than 2.5 million people worldwide. The disease progression is likely to be the result of neurodegeneration. Numerous therapies that have emerged to treat relapsing forms of MS have been unsuccessful in slowing or halting progressive forms of the disease, during which inflammatory activity is replaced by axonal loss and atrophy. BDNF-AS is a type of long non-coding RNAs that has a negative transcriptional regulation over the neurotrophin BDNF, which is known to be highly expressed in actively demyelinating MS lesions and which has a function in neuron survival and plasticity necessary for neuroprotection during inflammation. BDNF has been shown to be low in older and chronic MS plaques, which could be a contributing factor to the ongoing degenerative changes in the chronic progressive stages of MS. However, few studies have investigated the role of BDNF-AS and how it may contribute to the role of BDNF in MS. Therefore, we studied the relative expression of BDNF-AS in the serum of patients with different disease types of MS via qRT-PCR. We found that BDNF-AS is significantly downregulated in MS as compared to controls. We also determined a relative expression cut-off of (0.31) fold change, which can be used for the diagnosis of MS with high specificity and sensitivity.

Multiple sclerosis (MS) is a complicated condition in which the immune system attacks myelinated axons in the central nervous system (CNS), destroying both myelin and axons to varying degrees. Several environmental, genetic, and epigenetic factors influence the risk of developing the disease and how well it responds to treatment. Cannabinoids have recently sparked renewed interest in their therapeutic applications, with growing evidence for their role in symptom control in MS. Cannabinoids exert their roles through the endogenous cannabinoid (ECB) system, with some reports shedding light on the molecular biology of this system and lending credence to some anecdotal medical claims. The double nature of cannabinoids, which cause both positive and negative effects, comes from their actions on the same receptor. Several mechanisms have been adopted to evade this effect. However, there are still numerous limitations to using cannabinoids to treat MS patients. In this review, we will explore and discuss the molecular effect of cannabinoids on the ECB system, the various factors that affect the response to cannabinoids in the body, including the role of gene polymorphism and its relation to dosage, assessing the positive over the adverse effects of cannabinoids in MS, and finally, exploring the possible functional mechanism of cannabinoids in MS and the current and future progress of cannabinoid therapeutics.