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P1‐212: MICROGLIAL INTERACTIONS WITH AMYLOID PLAQUES ARE MODULATED BY SEX AND APOE GENOTYPE IN EFAD MICE
Author(s) -
Stephen Terri,
Cacciottolo Mafalda,
Balu Deebika,
Morgan Todd E.,
Ladu Mary Jo,
Finch Caleb E.,
Pike Christian J.
Publication year - 2019
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.2019.06.767
Subject(s) - microglia , trem2 , apolipoprotein e , neuroinflammation , senile plaques , biology , phagocytosis , pathology , amyloid (mycology) , pathogenesis , immunology , alzheimer's disease , inflammation , medicine , disease
compromised by mutations located in the extracellular domain. The PTC variant p.Q230*, showed a complete loss of expression on the cell membrane. The majority of the patient specific missense variations showed a spectrum of reduced expression indicating destabilization of DPP6. Investigation of DPP6Kv4.2 protein expression levels showed that DPP6 was significantly decreased in C9orf72 carriers (p1⁄40.0001) and Kv4.2 was significantly reduced in GRN (p<0.0001), C9orf72 (p1⁄40.0059) and VCP (p<0.0001) carriers. Conclusions: Our results suggest that neuronal loss of the DPP6-Kv4.2 complex could be a shared event in brain neurodegeneration warranting further investigation. Interactome analysis will identify additional interacting partners of DPP6 and will further clarify its molecular signature.