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Review
.2014 Jun 15;7(7):3504-11.
eCollection 2014.

Is apolipoprotein E4 an important risk factor for vascular dementia?

Affiliations
Review

Is apolipoprotein E4 an important risk factor for vascular dementia?

Troy T Rohn. Int J Clin Exp Pathol..

Abstract

Despite the fact that vascular dementia (VaD) represents the seconding leading cause of dementia in the USA, behind only Alzheimer's disease (AD), there remains a lack of consensus on the pathological criteria required for diagnosis of this disease. A number of clinical diagnostic criteria exist but are poorly validated and inconsistently applied. It is clear that vascular risk factors play an important role in the etiology of VaD, including hypertension, stroke, diabetes, and atherosclerosis. Vascular risk factors may increase the risk for VaD by promoting inflammation, cerebral vascular disease, white matter lesions, and hippocampal sclerosis. Because vascular risk factors seem to impart a high degree of risk for conferring VaD, it seems logical that the apolipoprotein E (APOE) status of individuals may be important. APOE plays a critical role in transporting cholesterol in and out of the CNS and in AD it is known that harboring the APOE allele increases the risk of AD perhaps due to the improper functioning of this protein. The purpose of this review is to examine the important pathological features and risk factors for VaD and to provide a critical assessment of the current literature regarding whether or not apoE4 also confers disease risk in VaD. The preponderance of data suggests that harboring one or both APOE4 alleles elevates the risk for VaD, but not to the same extent as found in AD.

Keywords: Alzheimer’s disease; Apolipoprotein E4 (APOE4); blood brain barrier; inflammation; neurofibrillary tangles; pathology; risk factors; vascular dementia.

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Figures

Figure 1
Figure 1
Overlap between AD and VaD is a common and often confounding factor in diagnosing VaD. The available evidence suggests that up to 20-30 percent of patients meeting pathological criteria for VaD also have concurrent AD pathology. This co-occurrence of symptoms between the two diseases has led to a lack of consensus about the best clinical criteria to identify VaD compounding the probability of misdiagnosing VaD as AD. Therefore, clear clinical and pathological criteria for the diagnosis of VaD will be critical in differentiating pure VaD from AD and mixed dementia.
Figure 2
Figure 2
Overview of the known major pathological features and risk factors associated with VaD. A key feature of VaD is the presence of cerebral vasculature lesions that may lead to inadequate blood flow to neurons. Depending on the site of these lesions, neuronal degeneration may produce symptoms of dementia. The potential risk factors that may trigger the pathological processes associated with VaD are shown, with many of these being important cardiovascular risk factors as well. See main text for details.
Figure 3
Figure 3
Evidence for apoE immunoreactive pathology in the human VaD brain. (A) Representative labeling utilizing a custom, in house antibody that specifically detects the amino-terminal fragment of apoE shows the presence of immunoreactivity within apparent NFTs in postmortem VaD brain tissue sections (arrows, A). (B) Confirmation of cleaved apoE within NFTs was confirmed following double-label immunofluorescence experiments with the cleaved apoE antibody (green) co-localizing with the tangle marker, PHF-1 (red), (arrow, B). Our custom apoE cleavage antibody also revealed punctate labeling within blood vessels. (C) Cleaved apoE was not evident within extracellular beta-amyloid plaques, although full-length APOE was readily present following co-localization with antibodies to full-length apoE4 (red) and an anti-Ab antibody, 6E10 (green). (D) For details on these findings, please see the original article [66]. All scale bars represent 10 μm.
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