For a study, it was determined that immune dysregulations and a compromised skin barrier, which included changes in lipid organization, were hallmarks of atopic dermatitis (AD). β- glucocerebrosidase (GBA) facilitated the translation of glucosylceramide (GlcCER) into ceramide (CER) and cholesterol into glucose cholesterol (GlcChol) in the stratum corneum (SC). Skin barrier deficiencies in Alzheimer’s disease might have been caused by changes in GBA activity. GBA activity in the SC of children with Alzheimer’s disease before and after topical corticosteroid therapy and comparisons with healthy controls. GlcCER and CER containing hydroxysphingosine base (GlcCER[H] and CER[H], respectively) and GlcChol SC levels were determined. After that, they would have been compared with disease severity, skin barrier function, and the local cytokine environment. Before and after 6 weeks of topical corticosteroid therapy, lipid markers and cytokines of innate, Th-1, and Th-2 immunity were measured in the SC of healthy children and clinically intact skin of children with AD. SCORAD was used to determine the severity of Alzheimer’s disease, while TEWL was used to determine skin barrier function. Baseline GBA activity and GlcChol levels in AD youngsters were higher, but the levels decreased after treatment. In AD, the CER[H] and CER[H] /GlcCER[H] ratios were both elevated. GBA activity and GlcChol levels were linked to TEWL and numerous cytokines, including IL1α and IL-18. GlcChol was found to be highly linked to illness severity. In AD, researchers found increased GBA activity and GlcChol levels. The results implied that inflammation played a significant role in lipid processing problems. GBA activity or GlcChol could have been effective biomarkers for tracking therapy responses in Alzheimer’s disease.
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