Authors
Jeffrey Thompson, Department of Neurology, University of New Mexico School of Medicine, Albuquerque, NM, 87131, United States; Memory and Aging Center, University of New Mexico School of Medicine, Albuquerque, NM, 87131, United States
Yirong Yang, College of Pharmacy, University of New Mexico School of Medicine, Albuquerque, NM, 87131, United States
Kelsey Duval
Karen SantaCruz, Department of Pathology, University of New Mexico School of Medicine, Albuquerque, NM, 87131, United States
Michael Griego, Department of Neurology, University of New Mexico School of Medicine, Albuquerque, NM, 87131, United States
Haojie Chen, Department of Neurology, University of New Mexico School of Medicine, Albuquerque, NM, 87131, United States
Haoran Deng, Department of Neurology, University of New Mexico School of Medicine, Albuquerque, NM, 87131, United States
Carlos Perez, Department of Neurology, University of New Mexico School of Medicine, Albuquerque, NM, 87131, United States
Sean Maez, Department of Neurology, University of New Mexico School of Medicine, Albuquerque, NM, 87131, United States
Sasha Hobson, Department of Neurology, University of New Mexico School of Medicine, Albuquerque, NM, 87131, United States; Memory and Aging Center, University of New Mexico School of Medicine, Albuquerque, NM, 87131, United States
Theodore Li, Department of Neurology, University of New Mexico School of Medicine, Albuquerque, NM, 87131, United States
Halima Akter, Department of Neurology, University of New Mexico School of Medicine, Albuquerque, NM, 87131, United States
Michel Torbey, Department of Neurology, University of New Mexico School of Medicine, Albuquerque, NM, 87131, United States
Yi Yang, Department of Neurology, University of New Mexico School of Medicine, Albuquerque, NM, 87131, United States
Publication Date
3-22-2024
Abstract
Cerebral Small Vessel Disease (SVD) contributes to 50% of human dementias world-wide. Human studies indicate a causative role of microvascular endothelial dysfunction, including blood-brain barrier (BBB) dysfunction in SVD. A potential link between BBB dysfunction and tissue hypoxic hypoperfusion underlying the essentials of SVD has been postulated; however, the mechanism(s) remains an open question. This study proposes the reversal of BBB disruption through pharmacological intervention of S1PR1 signaling as a novel therapeutic target for SVD.
Funding: This study is supported by a NIH/NINDS grant (1RF1NS110724) and a UNM MOS RAC grant to Dr. Yi Yang.
Recommended Citation
Thompson, Jeffrey; Yirong Yang; Kelsey Duval; Karen SantaCruz; Michael Griego; Haojie Chen; Haoran Deng; Carlos Perez; Sean Maez; Sasha Hobson; Theodore Li; Halima Akter; Michel Torbey; and Yi Yang.
"Selectively targeting S1PR1 restores BBB integrity and attenuates SVD-related neuropathological progression in a rat model of chronic hypoxic hypoperfusion."
(2024).
https://digitalrepository.unm.edu/hsc-bbhrd/177
