/3Amyloid protein deposition inthebrain after severe headinjury: implications forthe pathogenesis ofAlzheimer's disease

In a recentpreliminary studyitwas reportedthata severehead injury resulted inthedeposition ofpfamyloid protein(pAP)inthecortical ribbonof 30/oofpatients whosurvived forless than twoweeks.Multiple cortical areashave now beenexaminedfrom152patients (agerange8 weeks-81years)aftera severeheadinjury withasurvival timeof betweenfourhoursand25years.This series wascomparedwitha groupof44 neurologically normal controls(age range51to80years). Immunostaining withan antibody to8APconfirmed the original findings that30%ofcasesofhead injury have8APdeposits inoneormore cortical areas.Increasing ageseemedto accentuate theextentof8APdeposition and potential correlations withother pathological changesassociated with headinjury werealsoinvestigated. In addition, a amyloidprecursorprotein (IAPP)immunoreactivity wasincreased intheperikarya ofneuronsinthevicinity of/APdeposits. Thedatafromthisstudy support proposals thatincreased expressionof8APPispartofan acutephase response toneuronal injury inthehuman brain, thatextensive overexpression of /lAPPcanleadtodeposition of/APand theinitiation ofan Alzheimer diseasetypeprocess withindays,andthathead injury may beanimportant aetiological factor inAlzheimer's disease.