Abstract
Dementia due to vascular disease results from ischemic infarctions affecting crucial areas of brain by virtue of their critical nature for memory, such as the hippocampus/dentate gyrus or dorsal medial nucleus of the thalamus; the aggregate mass of infarcts; and the bilateral involvement of cortical damage. However, the most important factor causing ischemic infarction is atherosclerotic vascular disease in both large and small arteries and arterioles. Since the best therapy for both strokes and vascular dementia is prevention, it follows that insights into the fundamental molecular biological mechanisms of atherosclerosis in patients with vascular dementia should provide clues for identifying genetic predisposition and planning rational therapeutic intervention. The hope and expectation is that the offending atherosclerotic changes can be prevented and reversed, thereby averting any ischemic brain injury and the potential for secondary dementia.
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© 1991 Springer-Verlag Berlin Heidelberg
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Yatsu, F.M. et al. (1991). Molecular Biology of Atherothrombotic Brain Infarction and Its Role in Vascular Dementia. In: Hartmann, A., Kuschinsky, W., Hoyer, S. (eds) Cerebral Ischemia and Dementia. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-76208-6_8
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DOI: https://doi.org/10.1007/978-3-642-76208-6_8
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