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Depression and Infl ammatory Signaling in Alzheimer Disease

Vascular signaling abnormalities in Alzheimer disease

Paula Grammas, PhD, Alma Sanchez, PhD, Debjani Tripathy, PhD, Ester Luo, PhD and Joseph Martinez
Cleveland Clinic Journal of Medicine August 2011, 78 (8 suppl 1) S50-S53; DOI: https://doi.org/10.3949/ccjm.78.s1.09
Paula Grammas
Garrison Institute on Aging and Department of Neurology, Texas Tech University Health Sciences Center, Lubbock, TX
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  • For correspondence: paula.grammas@ttuhsc.edu
Alma Sanchez
Garrison Institute on Aging and Department of Neurology, Texas Tech University Health Sciences Center, Lubbock, TX
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Debjani Tripathy
Garrison Institute on Aging and Department of Neurology, Texas Tech University Health Sciences Center, Lubbock, TX
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Ester Luo
Garrison Institute on Aging and Department of Neurology, Texas Tech University Health Sciences Center, Lubbock, TX
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Joseph Martinez
Garrison Institute on Aging and Department of Neurology, Texas Tech University Health Sciences Center, Lubbock, TX
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ABSTRACT

Our laboratory has documented that brain microvessels derived from patients with Alzheimer disease (AD) express or release a myriad of factors that have been implicated in vascular activation and angiogenesis. In addition, we have documented that signaling cascades associated with vascular activation and angiogenesis are upregulated in AD-derived brain microvessels. These results are consistent with emerging data suggesting that factors and processes characteristic of vascular activation and angiogenesis are found in the AD brain. Despite increases in proangiogenic factors and signals in the AD brain, however, evidence for increased vascularity in AD is lacking. Cerebral hypoperfusion/hypoxia, a potent stimulus for vascular activation and angiogenesis, triggers hypometabolic, cognitive, and degenerative changes in the brain. In our working model, hypoxia stimulates the angiogenic process; yet, there is no new vessel growth. Therefore, there are no feedback signals to shut off vascular activation, and endothelial cells become irreversibly activated. This activation results in release of a large number of proteases, inflammatory proteins, and other gene products with biologic activity that can injure or kill neurons. Pathologic activation of brain vasculature may contribute noxious mediators that lead to neuronal injury and disease processes in AD brains. This concept is supported by preliminary experiments in our laboratory, which show that pharmacologic blockade of vascular activation improves cognitive function in an animal model of AD. Thus, “vascular activation” could be a novel, unexplored therapeutic target in AD.

Footnotes

  • All authors reported that they have no financial relationships that pose a potential conflict of interest with this article.

  • This work was supported in part by grants from the National Institutes of Health (AG15964, AG020569 and AG028367). Dr. Grammas is the recipient of the Shirley and Mildred Garrison Chair in Aging.

  • © 2011 The Cleveland Clinic Foundation. All Rights Reserved
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Cleveland Clinic Journal of Medicine: 78 (8 suppl 1)
Cleveland Clinic Journal of Medicine
Vol. 78, Issue 8 suppl 1
1 Aug 2011
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Vascular signaling abnormalities in Alzheimer disease
Paula Grammas, Alma Sanchez, Debjani Tripathy, Ester Luo, Joseph Martinez
Cleveland Clinic Journal of Medicine Aug 2011, 78 (8 suppl 1) S50-S53; DOI: 10.3949/ccjm.78.s1.09

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Vascular signaling abnormalities in Alzheimer disease
Paula Grammas, Alma Sanchez, Debjani Tripathy, Ester Luo, Joseph Martinez
Cleveland Clinic Journal of Medicine Aug 2011, 78 (8 suppl 1) S50-S53; DOI: 10.3949/ccjm.78.s1.09
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