Abstract

The apolipoprotein E gene (Apo E) is located on the 19th chromosome and has 3 alleles, which are e2, e3, and e4.1 Previous studies showed that the Apo E e4 allele is a risk factor that increases the risk of sporadic Alzheimer’s disease (AD) and late-onset AD in addition to decreasing the age of onset. Although disputable, some studies have suggested that Apo E e4 is related to a high level of low density lipoprotein and may affect nervous system diseases associated with vascular injuries.2,3 Also, vascular pathology has been repeatedly reported in late-stage AD patients. It is also reported that cerebrovascular and cardiovascular risk factors can enhance the progress of AD. In this way, many recent studies have suggested that vascular factors may be common etiologic factors of both AD and vascular dementia (VaD).4 Subcortical vascular dementia (SVaD) is known to be caused by microangiopathy within the deep brain. SVaD can be divided into arteriosclerotic leukoencephalopathy (Binswanger type), which contains the etiologic factor in the white matter, and multiple subcortical lacunar lesion (lacunar type), which is caused by multiple infarction of deep brain gray matter. Likewise, considering the effect of Apo E e4 lipid metabolism and the common vascular etiologic factor found in AD A Comparison of Apolipoprotein E Polymorphism in Alzheimer’s Disease and Subcortical Vascular Dementia in Koreans

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