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• W2980744252 abstract "Alzheimer's disease (AD) is hypothesized to start with amyloid aggregation, followed by tau pathology. However, 25% of the symptomatic patients with AD have normal CSF tau levels. Tau stabilizes axonal microtubules and increased tau levels are supposed to reflect axonal damage. Recent studies showed that tau is also located in dendrites, released during synaptic activity, and is associated with plasticity. To clarify the role of tau in early AD we performed a CSF proteomic and genetic study. We selected AD individuals in preclinical, prodromal or dementia stage with abnormal CSF abeta42 (a+) and abnormal CSF total tau (a+t+, n=572) or normal total tau (a+t-, n=785) and controls with normal cognition and normal abeta42 and tau (a-t-, n=400) from ADNI and EMIF-AD multimodality biomarker discovery study with proteomic or GWAS data available. ADNI performed targeted proteomics (n=270, 254 proteins included). EMIF-AD performed immunoassays of established AD markers and untargeted mass spectroscopy (n=310, 1466 proteins included). We calculated polygenic risk scores (PGRS) based on IGAP weights in the pooled ADNI and EMIF-AD cohorts (n=1109). In both cohorts, a+t+ and a+t- groups showed opposite CSF patterns. In the a+t+ group more proteins were increased than decreased relative to controls (Increased: EMIF:479 (33% of all proteins measured); ADNI:131 (52%); Decreased EMIF:44 (3%); ADNI:3 (1%)). In the a+t- group, more proteins were decreased than increased (Decreased: EMIF:413 (28%); ADNI:108 (43%); Increased: EMIF:60 (4%); ADNI:7 (3%)). Half of the proteins increased in a+t+ were decreased in a+t- (figure 1). Increased proteins in the a+t+ group were associated with neuronal plasticity, abeta production, MAPK signalling, microglia activation, and apoptosis. In the a+t- group, decreased proteins were associated with neuronal plasticity and increased proteins were associated with blood-brain and blood-CSF barrier dysfunction. Hyperplasticity in a+t+ and hypoplasticity in a+t- were already present in preclinical AD. Both a+t+ and a+t- groups had higher PGRS's than controls (p=1.4*10−7-6.8*10−21), and a+t+ had higher PGRS's than a+t- (p=0.02−0.04, figure 2)." @default.
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• W2980744252 date "2019-07-01" @default.
• W2980744252 modified "2023-10-18" @default.
• W2980744252 title "P4-525: ASSOCIATION OF CSF TAU WITH HYPERPLASTICITY IN ALZHEIMER'S DISEASE" @default.
• W2980744252 doi "https://doi.org/10.1016/j.jalz.2019.08.072" @default.
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