Clinical Neuroscience and NeuropathologyA β42 is the predominant form of amyloid b -protein in the brains of short-term survivors of head injuryGentleman, Stephen M.1,6; Greenberg, Barry D.2; Savage, Mary J.2; Noori, Muna1; Newman, Suzanna J.3; Roberts, Gareth W.3; Griffin, W Sue T.4; Graham, David I.5Author Information 1Department of Anatomy, Charing Cross & Westminster Medical School, St Dunstan's Road, London, W6 8RP, UK 2Cephalon Inc, 145 Brandywine Parkway, West Chester, PA 193804245, USA 3SmithKline Beecham Pharmaceuticals, Molecular Neuropathology Research, New Frontiers Science Park, Third Avenue, Harlow, Essex, CM19 5AW, UK 4McLellan Veterans Affairs Medical Center, 4300 W. 7th St, Little Rock, AR 72205, USA 5Department of Neuropathology, Institute of Neurological Sciences, Southern General Hospital, Glasgow, G51 4TF, UK 6Corresponding Author: Stephen M. Gentleman ACKNOWLEDGEMENTS: Funded in part by NIH grant AG12411. S.M.G. was an Alzheimer's Disease Society Research Fellow. M.N. was funded on a Wellcome Trust Vacation Scholarship. Received 28 January 1997: accepted 19 February 1997 NeuroReport: April 14, 1997 - Volume 8 - Issue 6 - p 1519-1522 Buy Abstract FATAL head injury results in the formation of diffuse parenchymal deposits of amyloid β-protein (Aβ) in the brains of approximately 30% of individuals. We used carboxyl terminal-specific antisera to examine the exact nature of these deposits in paraffin sections of neocortex from seven head-injured patients. Immunostaining for Aβ42 was observed in all parenchymal deposits whereas staining for Aβ40, the form of the protein which predominates in serum and cerebrospinal fluid, was seen in only a small proportion of deposits. The relative paucity of Aβ40 suggests that post-traumatic deposits do not arise as a result of passive leakage from damaged cerebral blood vessels but are similar to the early Aβ42 parenchymal deposits seen in Down's syndrome and Alzheimer's disease. © Lippincott-Raven Publishers.