Candan Depboylu

TL;DR: Evidence is provided for a more detailed investigation of IVIgG for the treatment of AD as evidence for active or passive immunisation can mitigate plaque pathology in murine models of Alzheimer's disease.

Abstract: There is increasing evidence that immune mechanisms are involved in the pathogenesis of Alzheimer's disease (AD). Recently, polymorphisms of the interleukin (IL)-1 and IL-6 genes were found to be associated with late-onset AD. The immunoregulatory IL-10 downregulates synthesis of pro-inflammatory cytokines such as IL-1. Current evidence suggests that some polymorphisms in the IL-10 promoter may have functional effects on IL-10 transcription. A total of 406 German AD patients (mean age 70.2+/-10.0 years, range 50-95 years, 42% female) and 251 unrelated non-demented control subjects (mean age 66.8+/-10.6 years, range 50-93 years, 38% female) were investigated for the presence of three polymorphisms in the IL-10 promoter region (-1087A/G, -824C/T, -597C/A). No significant differences in the allelic distribution of the analyzed IL-10 polymorphisms have been found between AD patients and controls. We conclude that polymorphisms in the IL-10 promoter region do not increase the risk of developing AD.

TL;DR: It is concluded that IL-6 (–174) polymorphism does not influence the risk of developing AD in the cohort of AD patients analysed.

TL;DR: It is concluded that the C/T polymorphism in the IL-1alpha promoter region at -889 does not increase the risk to develop Parkinson's disease and no significant difference in the allelic distribution has been found between PD and controls.

TL;DR: The presence of VMAT2 in epidermal Langerhans cells revealed a previously unrecognized monoamine-handling phenotype of these cells and indicates possible involvement of amine storage and release associated with antigen presentation.