F1‐01‐02: Tackling overlap of neuropsychiatric symptoms in Alzheimer's and other dementias: Toward a unified approach to evaluation and treatment

With the exception of a small number of familial forms the causes for FTLD are unknown. With our plasma proteomics approach we identified novel disease pathways that may open possibilities for treatment and diagnostics.Methods:We employed medium scale plasma proteomics, measuring more than 600 soluble cellular communication factors in plasma from control (n 1⁄4 83) and FTLD (n 1⁄4 92) patients with semantic dementia, as well as from FTLD patients with a familial Progranulin mutation (n 1⁄4 24). We are using an antibody microarray based approach in combination with statistical and computational tools to identify altered pathways. Results: Our analysis revealed a deregulation of inflammatory markers, most prominently in the TNF-alpha and IL-1 pathways. We further confirmed an increase in TNF-alpha in the plasma of FTLD patients by ELISA. Currently we are in the process of analyzing the immune phenotype of FTLD patients and comparing it to healthy controls. Conclusions: Our results show evidence for a novel immune phenotype in FTLD patients with TDP-43 pathology. This opens up possibilities for a targeted anti-inflammatory therapy for this disease.