One of the most frequent inflammatory skin conditions is atopic dermatitis (AD). Alzheimer’s disease is caused by barrier dysfunction and abnormal immunological activation of T helper (Th) 2 and Th22 cells, as well as varying degrees of Th1 and Th17 cells in distinct subtypes. The Janus kinase (JAK)–signal transducer and activator of transcription (STAT) and spleen tyrosine kinase (SYK) pathways are involved in the signaling of several AD-related cytokines, including IFN-γ, IL-4, IL-13, IL-31, IL-33, IL-23, IL-22, and IL-17, and mediate downstream inflammation and barrier changes.
While Th2-driven, the clinical and biochemical variety of AD endotypes underscores the unmet need for effective therapeutic approaches that target more than one immune axis and are safe for long-term use. JAK inhibitors have overlapping but separate modes of action and safety profiles because they target various combinations of kinases. Several topical and oral JAK inhibitors have been demonstrated to reduce the severity and symptoms of Alzheimer’s disease.
A review of the JAK and SYK inhibitors now being tested for effectiveness and safety in the treatment of Alzheimer’s disease highlights existing evidence on a promising area of therapies and elucidates the intricate molecular relationships that drive Alzheimer’s disease.
Reference:link.springer.com/article/10.1007/s40257-018-0413-2
