P3-197: Cystic borrelia in Alzheimer’s disease and in non-dementia neuroborreliosis

Abstract

specific antigens (p62, HLA-DR, GFAP, NeuN), heat-shock proteins (HSP), and cytoskeletal components. Stereologic point-counting techniques and Western blotting were used to quantify neuronal loss and soluble tau protein, respectively. Results: Clinically, 8 patients had FTLD. Behavioral problems and aphasia were an important finding and at least three patients suffered from parkinsonian features. No mutations were identified in MAPT, APP, PS1, PS2, and PRNP. We showed frontotemporal atrophy with filamentous Ub-positive intracellular inclusions in absence of tau pathology or any alterations in the levels of soluble tau. We characterized their cellular and subcellular localization and morphology. Ub-positive inclusions predominantly occurred within neurons ( 97%), but were also observed within oligodendroglia (approx. 2%), microglia ( 1%), but not within astroglia. Regarding the subcellular localization, the intranuclear inclusions (INI) were up to approx. 4 fold more frequent than the cytoplasmic inclusions, although the latter were more specific to neurons. The INIs frequently appeared spindle-shaped and 3-D confocal reconstructions identified flattened, leaf-like structures. Ultrastructurally, straight 10-18 nm diameter filaments constituted the spindle-shaped inclusions that occurred in close proximity to the nuclear membrane. Staining for HSP40, p62, and valosin/p97 was observed in only a minority of the inclusions. Conclusion: While the precise nature of the protein remains elusive, characterization of such familial FTLD-U patients would be helpful in identifying a common denominator in the pathogenesis of familial and the more prevalent sporadic FTLD-U.