Paulo W. Pires, PhD

Assistant Professor, Physiology
Assistant Professor, Physiological Sciences-GIDP
Assistant Professor Surgery
Research Interests

Research in the Pires laboratory focuses on the contributions of the brain vasculature to progression of cognitive impairment and dementia, including those seen during aging and Alzheimer’s Disease. We are particularly interested in understanding how misfolded proteins (such as amyloid-beta) affect ion channels responsible for control of brain blood vessels, and how these dysfunction may lead to reduced blood flow in the brain. Current projects in the lab are investigating the interplay between neuroinflammation and oxidative stress in impairment of potassium channels in the brain vasculature, how normal aging leads to impaired blood flow to the brain and the mechanisms by which excessive cellular cholesterol affects cerebral vascular regulation.

Degree(s)

  • 2004 BS Biological Sciences – Sao Paulo State University
  • 2007 M.S. Cell Biology – Campinas State University
  • 2013 Ph.D. Pharmacology and Toxicology – Michigan State University
  • 2018 Post-doctoral – University of Nevada
Publication Highlights

Josiane F Silva, Felipe D Polk, Andrea Savu, Allison M Kath, Michael T Gee, Paulo W Pires. BK Ca nitrosylation is associated with cerebral microvascular dysfunction in female 5x-FAD mice. bioRxiv. 2023 Jun 8:2023.06.06.543962. doi: 10.1101/2023.06.06.543962. Preprint

Jade A Blackwell, Josiane F Silva, Emma M Louis, Andrea Savu, Tally M Largent-Milnes, Heddwen L Brooks, Paulo W Pires. Cerebral arteriolar and neurovascular dysfunction after chemically induced menopause in mice. Am J Physiol Heart Circ Physiol. 2022 Nov 1;323(5):H845-H860. doi: 10.1152/ajpheart.00276.2022.

Emily C Peters, Michael T Gee, Lukas N Pawlowski, Allison M Kath, Felipe D Polk, Christopher J Vance, Juliana L Sacoman, Paulo W Pires. Amyloid- β disrupts unitary calcium entry through endothelial NMDA receptors in mouse cerebral arteries. J Cereb Blood Flow Metab. 2022 Jan;42(1):145-161. doi: 10.1177/0271678X211039592.