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[F4–07–03]: TAU OLIGOMERIC STRAINS IN SYNUCLEINOPATHIES
Author(s) -
Kayed Rakez
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.2017.07.400
Subject(s) - synucleinopathies , progressive supranuclear palsy , dementia with lewy bodies , in vivo , phenotype , disease , tau pathology , corticobasal degeneration , in vitro , lewy body , protein aggregation , biology , parkinson's disease , tau protein , neuroscience , dementia , alpha synuclein , microbiology and biotechnology , pathology , alzheimer's disease , medicine , biochemistry , genetics , gene
Background:Data from in vitro studies, tg animal models and from human post mortem studies suggest that amyloid beta (Ab), tau and alpha-synuclein (a-syn) may promote the aggregation of each other. For example, Ab induces phosporylation of a-syn at Ser129 in vitro (Swirski M et al, Alzheimer’s Res Ther 2014 6:77) and a-syn pathology influences the topographical distribution of tau (Walker L et al, Acta Neuropathol 129:729-48). Here, we quantitatively assessed Ab, tau and a-syn pathology in a large cohort of human post mortem brains to investigate possible correlations and identify areas where such correlations are most prevalent. Methods:Our study cohort consisted of 140 post mortem brains including Alzheimer’s disease (AD), Lewy body disease (LBD) and controls. Sections were stained with antibodies against Ab (4G8), tau (AT8) and a-syn (Novocastra). Quantitative assessment was based on automated image analysis and performed in 15 brain regions, covering a variety of neocortical and limbic areas. Results: In AD, controls and LDB significant (P<0.05) correlations were seen between Ab and tau loads, while no correlations were found between Ab and a-syn loads. In LBD cases tau loads significantly (P<0.01) correlated with a-syn loads in the entorhinal and cingulate cortex. Conclusions: Not surprisingly our data indicate an interaction between Ab and tau across all groups and further corroborates high AD pathology in LBD cases, where tau, but not Ab, seems to interact with a-syn to promote their aggregation. Further studies are warranted to understand the underlying mechanisms of these interactions and to clarify if tau triggers a-syn pathology in LBD. F4-07-02 INTERACTIONS OFABETA AND TAU IN SYNAPSE LOSS