beta-Amyloid (A beta)42(43), A beta 42, A beta 40 and apoE immunostaining of plaques in fatal head injury

Citation
K. Horsburgh et al., beta-Amyloid (A beta)42(43), A beta 42, A beta 40 and apoE immunostaining of plaques in fatal head injury, NEUROP AP N, 26(2), 2000, pp. 124-132
Citations number
46
Categorie Soggetti
Neurosciences & Behavoir
Journal title
NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY
ISSN journal
03051846 → ACNP
Volume
26
Issue
2
Year of publication
2000
Pages
124 - 132
Database
ISI
SICI code
0305-1846(200004)26:2<124:B(BAB4>2.0.ZU;2-C
Abstract
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 pr esence correlating strongly with possession of an apolipoprotein E (apoE)-e psilon 4 allele. The aim of the study was to investigate the relationship b etween A beta 42, A beta 40 and apoE immunostaining of A beta plaques in th e cerebral cortex and the relevance of apoE genotype in 23 fatally head-inj ured patients. These cases were known to have A beta deposits from a previo us 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 antibod y to apoE. A beta 42(43)-positive plaques were observed in all of the 23 ca ses and A beta 40 immunoreactivity in only 11 of the 23 cases. In addition, semiquantitative analysis showed that relatively fewer plaques were detect ed 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 a poE 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 apo E-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 a nd provide evidence that apoE is involved in the early stages of amyloid de position. Further, the findings may be of relevance to the role of apoE gen otype in influencing outcome after acute brain injury.