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PRECLINICAL PUBLICATION · 2019

Chronic synaptic insulin resistance after traumatic brain injury abolishes insulin protection from amyloid beta and tau oligomer-induced synaptic dysfunction

Rat / TBI

Evidence by therapy association

Study details and outcomes are extracted in the context of a specific intervention. Separate associations are retained rather than silently merged.

PMID 31160730 ↗2019Mixed findings

Chronic synaptic insulin resistance after traumatic brain injury abolishes insulin protection from amyloid beta and tau oligomer-induced synaptic dysfunction

RatTBIFluid percussionSprague-DawleyMaleEx vivo bath application to acute hippocampal slices and to isolated hippocampal synaptosomes; no in vivo systemic or intranasal administration was performed200 nM insulin for hippocampal slice electrophysiology and…Slice electrophysiology at 1 month and 3 months post-injury; synaptosomal insul…

Model: Moderate lateral (parasagittal) fluid percussion injury, using a 5 mm craniotomy 1 mm right of the sagittal suture midway between bregma and lambda, with injury delivered by a fluid percussion device

Hippocampal synapses became chronically insulin resistant after lateral fluid percussion injury, with significantly reduced insulin receptor responsiveness at 7 days, 1 month and 3 months post-injury in both hemispheres, reduced ipsilateral synaptic insulin receptor level at 7 days followed by an i…

Extraction: extract · Subtype source: rule · Supplied extraction confidence: 0.85. Machine-extracted fields require source verification.