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Frontal fibrosing alopecia (FFA) is a primary patterned cicatricial alopecia with a complicated pathogenesis yet to be fully understood. FFA appears to be increasing in incidence worldwide, especially in the last decade. In order to consider current treatment options, we reviewed current evidence for its pathogenesis comprising immune-mediated, genetic, hormonal and environmental factors. Th1-mediated inflammation with collapse of hair follicle immune privilege and bulge epithelial stem cell destruction, peroxisome proliferator-activated receptor gamma (PPAR-γ) depletion and epithelial–mesenchymal transition are key events leading to permanent hair follicle destruction in FFA. Although the vast majority of cases are sporadic, familial reports of FFA implicate genetic or epigenetic mechanisms in its pathogenesis. The frequent onset of FFA in post-menopausal women, similar patterning and co-existence with female pattern hair loss, together with a reportedly good response to 5α-reductase inhibitors suggest a role for sex steroid hormones. The reported increasing incidence invites speculation for, yet unproven, environmental triggers such as sun exposure and topical allergens. More robust research into this unique entity is required to help understand the complexity of the pathogenesis of FFA in order to find satisfactory therapeutic targets for this often distressing condition.  相似文献   
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Previous studies have implicated common and rare genetic variants as risk factors for late-onset Alzheimer's disease (LOAD). Here, weighted burden analysis was applied to over 10,000 exome-sequenced subjects from the Alzheimer's Disease Sequencing Project. Analyses were carried out to investigate whether rare variants predicted to have a functional effect within a gene were more commonly seen in cases or in controls. Confirmatory results were obtained for TREM2, ABCA7, and SORL1. Additional support was provided for PSEN1 (p = 0.0002), which previously had been only weakly implicated in LOAD. There was suggestive evidence that functional variants in PIK3R1, WNT7A, C1R, and EXOC5 might increase risk and that variants in TIAF1 and/or NDRG2 might have a protective effect. Overall, there was strong evidence (p = 5 × 10−6) that variants in tyrosine phosphatase genes reduce the risk of developing LOAD. Because PIK3R1 variants are expected to impair PI3K/Akt/GSK-3β signalling while variants in tyrosine phosphatase genes would enhance it, these findings are in line with those from animal models, suggesting that this pathway is protective against Alzheimer's disease.  相似文献   
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Journal of Autism and Developmental Disorders - This study investigated the association of child, caregiver, and caregiving measurements with the quality of life (QoL) in 81 caregivers (mostly...  相似文献   
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