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 axonal degeneration together with senile plaques (SP). SP are mainly composed of aggregated β amyloid (Aβ ), which are peptides derived from the amyloid precursor protein (APP). Apart from TBI in itself being considered a risk factor for AD, severe head injury seems to initiate a cascade of molecular events that are also associated with AD. We have therefore analysed the 42 amino acid forms of Aβ (Aβ (1- 42)) and two soluble forms of APP (α sAPP and β sAPP) in ventricular cerebrospinal fluid (VCSF) andAβ (1 42) in plasma from 28 patients in a serial samples 0 11 days after TBI. The levels of α sAPP, β sAPP and Aβ (1- 42) were determined using ELISA assays. After TBI, there was a signi ficant stepwise increase in VCSF Aβ (1- 42) up to 1173 % from day 0- 1 to day 5 6and inVCSF α sAPP up to 2033% increase from day 0 1 to day 7- 11. There was also a slight but significant increase of VCSF β sAPP from day 0- 1 to day 5- 6 and day 7- 11. By contrast, the plasma Aβ (1- 42) level is unchanged after injury. The marked increase in VCSF Aβ (1- 42) implies that increased Aβ expression may occur as a secondary phenomenon after TBI with axonal damage. The unchanged level of plasma Aβ (1- 42) in contrast to the marked increase in VCSF Aβ (1- 42) after severe TBI, supports the suggestion that plasma Aβ (1- 42) does not reflect Aβ metabolism in the central nervous system (CNS).
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 axonal degeneration together with senile plaques (SP). SP are mainly composed of aggregated β amyloid (Aβ ), which are peptides derived from the amyloid precursor protein (APP). Apart from TBI in itself being considered a risk factor for AD, severe head injury seems to initiate a cascade of molecular events that are also associated with AD. We have therefore analysed the 42 amino acid forms of Aβ (Aβ (1- 42)) and two soluble forms of APP (α sAPP and β sAPP) in ventricular cerebrospinal fluid (VCSF) andAβ (1 42) in plasma from 28 patients in a serial samples 0 11 days after TBI. The levels of α sAPP, β sAPP and Aβ (1- 42) were determined using ELISA assays. After TBI, there was a signi ficant stepwise increase in VCSF Aβ (1- 42) up to 1173 % from day 0- 1 to day 5 6and inVCSF α sAPP up to 2033% increase from day 0 1 to day 7- 11. There was also a slight but significant increase of VCSF β sAPP from day 0- 1 to day 5- 6 and day 7- 11. By contrast, the plasma Aβ (1- 42) level is unchanged after injury. The marked increase in VCSF Aβ (1- 42) implies that increased Aβ expression may occur as a secondary phenomenon after TBI with axonal damage. The unchanged level of plasma Aβ (1- 42) in contrast to the marked increase in VCSF Aβ (1- 42) after severe TBI, supports the suggestion that plasma Aβ (1- 42) does not reflect Aβ metabolism in the central nervous system (CNS).
出处
《世界核心医学期刊文摘（神经病学分册）》
2005年第1期14-15,共2页
Digest of the World Core Medical Journals:Clinical Neurology
