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