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Role of Vascular Risk Factors and Vascular Dysfunction in Alzheimer's Disease
Abstract
Recent findings indicate that vascular risk factors and neurovascular dysfunction play integral roles in the pathogenesis of Alzheimer's disease. In addition to aging, the most common risk factors for Alzheimer's disease are apolipoprotein e4 allele, hypertension, hypotension, diabetes, and hypercholesterolemia. All of these can be characterized by vascular pathology attributed to conditions such as cerebral amyloid angiopathy and subsequent blood‐brain barrier dysfunction. Many epidemiological, clinical, and pharmacotherapeutic studies have assessed the associations between such risk factors and Alzheimer's disease and have found positive associations between hypertension, hypotension, and diabetes mellitus. However, there are still many conflicting results from these population‐based studies, and they should be interpreted carefully. Recognition of these factors and the mechanisms by which they contribute to Alzheimer's disease will be beneficial in the current treatment regimens for Alzheimer's disease and in the development of future therapies. Here we discuss vascular factors with respect to Alzheimer's disease and dementia and review the factors that give rise to vascular dysfunction and contribute to Alzheimer's disease. Mt Sinai J Med 77:82&–102, 2010. © 2010 Mount Sinai School of Medicine
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Vascular risk factors and neurovascular dysfunction play integral roles in the pathogenesis of AD.
“Atherosclerosis has been associated with AD and cerebral angiopathy in humans [43], [44], and recent findings indicate that vascular risk factors and neurovascular dysfunction play integral roles in the pathogenesis of AD [45].”
From ApoB100/LDLR-/- Hypercholesterolaemic Mice as a Model for Mild Cognitive Impairment and Neuronal Damage (2011) · cites this paper as [45]
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Sorted by citations
Biron, K. E., Dickstein, D. L., Gopaul, R., & Jefferies, W. A. (2011) · PLoS ONE · doi:10.1371/journal.pone.0023789 · Cited by 300
Self-citationGetting to the Heart of Alzheimer Disease
Tublin, J. M., Adelstein, J. M., del Monte, F., Combs, C. K., & Wold, L. E. (2019) · Circulation Research · doi:10.1161/circresaha.118.313563 · Cited by 188
Endothelin-1 is Elevated in Alzheimer's Disease and Upregulated by Amyloid-β
Palmer, J. C., Barker, R., Kehoe, P. G., & Love, S. (2012) · Journal of Alzheimer's Disease · doi:10.3233/jad-2012-111760 · Cited by 110
Prevention of age-related changes in hippocampal levels of 5-methylcytidine by caloric restriction
Chouliaras, L., van den Hove, D. L. A., Kenis, G., Keitel, S., Hof, P. R., van Os, J., Steinbusch, H. W. M., Schmitz, C., & Rutten, B. P. F. (2012) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2011.06.003 · Cited by 78
Self-citationThe Framingham Brain Donation Program: Neuropathology Along the Cognitive Continuum
Au, R., Seshadri, S., Knox, K., Beiser, A., J. Himali, J., J. Cabral, H., Auerbach, S., C. Green, R., A. Wolf, P., & C. McKee, A. (2012) · Current Alzheimer Research · doi:10.2174/156720512801322609 · Cited by 65
“Clinical and pathological studies suggest that concomitant vascular disease is common and determines the time of onset of clinical symptoms in persons with Alzheimer's disease pathology [62-66].”
BackgroundRamírez, C., Sierra, S., Tercero, I., Vázquez, J. A., Pineda, A., Manrique, T., & Burgos, J. S. (2011) · PLoS ONE · doi:10.1371/journal.pone.0022712 · Cited by 31
Bae, I.-S., Kim, J. M., Cheong, J. H., Ryu, J. I., & Han, M.-H. (2019) · Aging · doi:10.18632/aging.102316 · Cited by 22
Metadata
- Authors
- Dickstein, D. L., Walsh, J., Brautigam, H., Stockton, S. D., Gandy, S., & Hof, P. R.
- Venue
- Mount Sinai Journal of Medicine: A Journal of Translational and Personalized Medicine
- Publisher
- Wiley
- Published
- 2010-01
- Volume
- 77
- Issue
- 1
- Pages
- 82-102
- ISSN
- 0027-2507
- 1931-7581
- PMC
- PMC2918901
- Cited by
- 155
- References
- 40
- Language
- en
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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