Open AccessAssociation of Increased Cortical Soluble Aβ42 Levels With Diffuse Plaques After Severe Brain Injury in Humans
Author(s) -
Steven T. DeKosky,
Eric E. Abrahamson,
John R. Ciallella,
William R. Paljug,
Stephen R. Wisniewski,
Robert S. B. Clark,
Miloš D. Ikonomović
Publication year - 2007
Publication title -
archives of neurology
Language(s) - English
Resource type - Journals
eISSN - 1538-3687
pISSN - 0003-9942
DOI - 10.1001/archneur.64.4.541
Subject(s) - traumatic brain injury , apolipoprotein e , medicine , pathology , alzheimer's disease , head injury , disease , endocrinology , surgery , psychiatry
Traumatic brain injury (TBI) is an environmental risk factor for developing Alzheimer disease. This may be due, in part, to changes associated with beta-amyloid (Abeta) plaque formation, which can occur within hours after injury, regardless of the patient's age. In addition to being precursors of toxic fibrils that deposit into plaques, soluble (nonfibrillar) Abeta peptides are posited to disrupt synaptic function and are associated with cognitive decline in Alzheimer disease. Changes in soluble Abeta levels and their relationship to Abeta plaque formation following TBI are unknown.
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