Marked increase of ?-amyloid(1?42) and amyloid precursor protein in ventricular cerebrospinal fluid after severe traumatic brain injury
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 [beta]-amyloid (A[beta]), which are p...
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Veröffentlicht in: | Journal of neurology 2004-07, Vol.251 (7), p.870 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | 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 [beta]-amyloid (A[beta]), 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 A[beta] (A[beta] |
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ISSN: | 0340-5354 1432-1459 |
DOI: | 10.1007/s00415-004-0451-y |