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[O2–15–05]: ALPHA‐SYNUCLEIN OLIGOMERS INDUCE MEMORY IMPAIRMENT INFLUENCED BY RAPID GLIAL CELL ACTIVATION
Author(s) -
Forloni Gianluigi,
La Vitola Pietro,
Cerovic Milicia,
Albani Diego,
Pollegioni Loriano,
Balducci Claudia
Publication year - 2017
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2017.07.233
Subject(s) - microglia , long term potentiation , neuroscience , tlr4 , memory impairment , hippocampus , hippocampal formation , extracellular , biology , chemistry , microbiology and biotechnology , inflammation , signal transduction , receptor , immunology , biochemistry , cognition
age-matched controls) were immunostained for markers of neuropathology (a-synuclein, amyloid-b, p-tau), microglial activation (Iba1, HLA-DR, CD68) and FcgRs (CD64, CD32a, CD32b and CD16). Quantification was performed to obtain protein load (%) using Image J. b) Clinical biomarker study: 90 participants (30 DLB, 30 AD, 30 controls) are entering an observational, cross-sectional study. ELISA and flow cytometry are being used to investigate blood markers of systemic inflammation. Results: a) In the DLB brain there was significantly higher a-synuclein and amyloid-b (p1⁄40.039) protein load, with a trend for higher p-tau (p1⁄40.052) load, compared to controls. No significant difference was found in the load of microglial activation markers Iba1 (p1⁄40.307), HLA-DR (p1⁄40.832) or CD68 (p1⁄40.064). However, FcgR markers did show significantly decreased CD32a (p1⁄40.043) and increased CD16 load (p1⁄40.027) in DLB compared to controls, but there was no difference in CD64 (p1⁄40.582) or CD32b load (p1⁄40.976). No significant correlations were found between any neuropathological and any inflammatory marker in either cohort. b) Clinical study is due to complete in 2017. Conclusions:Despite the confirmation of increased neuropathology in the DLB brain, this did not appear to affect the expression of microglia, as previously seen in AD. However, the FcgR profile does appear to be modified in DLB. Ongoing work aims to investigate systemic inflammation in the clinical study, with the potential for identification of a unique inflammatory signature in DLB.