β-Amyloid (Aβ)42(43), Aβ42, Aβ40 and apoE immunostaining of plaques in fatal head injury

beta-Amyloid (A beta) deposits are found in the brains of approximately one-third of patients who die within days after a severe head injury; their presence correlating strongly with possession of an apolipoprotein E (apoE)-epsilon 4 allele. The aim of the study was to investigate the relationship between A beta 42, A beta 40 and apoE immunostaining of A beta plaques in the cerebral cortex and the relevance of apoE genotype in 23 fatally head-injured patients. These cases were known to have A beta deposits from a previous study in which they were examined and semiquantified and related to apoE genotype. In the present study, the temporal cortex was probed using four different antibodies that recognize A beta 42(43), A beta 40 and an antibody to apoE. A beta 42(43)-positive plaques were observed in all of the 23 cases and A beta 40 immunoreactivity in only 11 of the 23 cases. In addition, semiquantitative analysis showed that relatively fewer plaques were detected with anti-A beta 40 than anti-A beta 42(43). ApoE-immunoreactive plaques were identified in 18 of the 23 cases. The number of plaques stained for apoE was relatively less than for A beta 42(43) but greater than for A beta 40. Furthermore, the density of A beta plaques detected using either A beta 42(43), A beta 40 or apoE antibodies was associated with possession of apoE-epsilon 4 in an allele dose-dependent manner. The results are consistent with A beta 42(43) as the initially deposited species in brain parenchyma and provide evidence that apoE is involved in the early stages of amyloid deposition. Further, the findings may be of relevance to the role of apoE genotype in influencing outcome after acute brain injury.