Marked increase of β-amyloid (1–42) and amyloid precursor protein in ventricular cerebrospinal fluid after severe traumatic brain injury

摘要: Severe traumatic brain injury (TBI) may result in widespread damage to axons, termed diffuse axonal injury. Alzheimer’s disease (AD) is characterised by synaptic and degeneration together with senile plaques (SP). SP are mainly composed of aggregated β-amyloid (Aβ), which peptides derived from the amyloid precursor protein (APP). Apart TBI itself being considered a risk factor for AD, severe head seems initiate cascade molecular events that also associated AD. We have therefore analysed 42 amino acid forms Aβ (Aβ(1–42)) two soluble APP (α-sAPP ssAPP) ventricular cerebrospinal fluid (VCSF) Aβ(1–42) plasma 28 patients serial samples 0–11 days after TBI. The levels α-sAPP, s-sAPP were determined using ELISA assays. After TBI, there was significant stepwise increase VCSF-Aβ(1–42) up 1173 % day 0–1 5–6 VCSF-β-sAPP 2033 7–11. There slight but By contrast, plasma- level unchanged marked VCSFAβ( 1–42) implies increased expression occur as secondary phenomenon damage. plasma-Aβ(1–42) contrast supports suggestion does not reflect metabolism central nervous system (CNS).