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In traumatic brain injury (TBI), the direct impact of the initial injury is followed by a cascade of events leading to more widespread cell death (secondary injury). These researchers examined in mice how amyloid-β protein (Aβ), a core component of Alzheimer disease pathology, contributes to the progression of neuronal loss after TBI.
After a controlled impact to the left parietal cortex, murine Aβ began accumulating, with levels increasing by 120% within 3 days and normalizing after a week. Aβ accumulation was accompanied by rising levels of amyloid precursor protein (APP) and of two enzymes involved in Aβ synthesis from APP (β-APP–cleaving enzyme-1 [Bace1] and γ-secretase). Deficits were observed in spatial learning (a hippocampal function…