White matter changes in early-onset Alzheimer's disease brains

• Published in: Geriatrics & gerontology international Vol. 4; no. 4; pp. 229 - 233
• Main Authors: Umahara, Takahiko, Tsuchiya, Kuniaki, Kiuchi, Akihiro, Kanaya, Kiyoshi, Iwamoto, Toshihiko, Takasaki, Masaru
• Format: Journal Article
• Language: English
• Published: Melbourne, Australia Blackwell Science Pty 01.12.2004; Blackwell Publishing Ltd
• Subjects: Alzheimer's disease; Brain; corpus callosum; Matter & antimatter; optic radiation; Wallerian degeneration; white matter
• ISSN: 1444-1586; 1447-0594
• DOI: 10.1111/j.1447-0594.2004.00252.x

Background:  The pathogenesis of white matter changes in Alzheimer's disease (AD) is not completely clear. Methods:  We histologically and immunohistochemically examined white matter lesions in 11 brains with early onset Alzheimer's disease. Results:  All 11 early onset AD brains had subcortical white‐matter pale lesions, but corpus callosum and optic radiation fibers were relatively well preserved. Some cases had severe white matter atrophy in the temporal lobe, and this is one cause of lateral ventricle inferior horn enlargement. Five of the 11 cases had white‐matter lesions without vascular changes, causing ischemic changes. It was difficult to clarify whether or not white‐matter changes were caused by secondary degeneration due to neuronal loss (Wallerian degeneration), because we could not explain why secondary degeneration occurred only in subcortical white matter excluding communicating fibers. Subcortical white‐matter beta protein deposits may not be associated with white‐matter lesions, because those beta deposits are located at marginal zones, while the myelin sheaths of those zones were relatively preserved. Conclusion:  We believe that some AD brains had definite white‐matter lesions without ischemic changes.