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Norris studies Alzheimer’s disease, a complex neurodegenerative disorder that affects tens of millions of people worldwide and for which there is no effective treatment. While the cause of this disease is still largely unknown, a large body of research implicates vascular dysfunction as a significant contributing factor. Alzheimer’s patients often present with brain hypoperfusion, a damaged cerebral vasculature, and abnormal hemostasis, and many patients also suffer from vascular disorders, such as diabetes and hypertension.

Norris has two main research interests. First, she studies the mechanistic impact of vascular comorbidities on Alzheimer’s pathogenesis. Her group has used an experimental model of hypertension in Alzheimer’s mice to suggest that high blood pressure in midlife exacerbates Alzheimer’s brain pathology by causing early neuroinflammation and damaging the blood-brain barrier. They have also defined the biochemical mechanisms that could explain the high incidence of hyperhomocysteinemia in Alzheimer’s patients. They are currently exploring the effects of dietary fat consumption and obesity on Alzheimer’s pathophysiology: Using Alzheimer’s mice, they have recently shown that eating certain fats early in life may be neuroprotective and therefore might prevent the onset of brain pathology and cognitive dysfunction.

Secondly, Norris is investigating the role of the plasma contact system in Alzheimer’s pathophysiology. Overactivation of this system can lead to blood clotting as well as inflammation, both of which are significant Alzheimer’s pathologies. Her team has shown an upregulation of contact system components in Alzheimer’s mouse models as well as human patients. They are exploring if an antibody that blocks the progression and positive feedback of this system could be beneficial to Alzheimer’s patients and other individuals that suffer from contact system dysfunction.