Research
Dr. Amy R. Nelson's lab is committed to eliminating Alzheimer's disease and related dementias. To do this, we seek to identify root causes of dementias and to determine whether interventions may be helpful in preventing and/or improving memory loss. We are scholars performing rigorous research to answer critical basic, translational and clinical research questions.
Pneumonia and the brain
Severe pneumonia causes incident dementia, and increases the risk of Alzheimer's disease. The Nelson lab has found that the Alzheimer's disease pathological player called tau also plays a role in the neurovascular changes caused by pneumonia in experimental models (Chaney et al., 2026, Commun Biol, and Lin et al., 2026, Am J Respir Cell Mol Biol). We are working to further understand shared and distinct roles of tau in pneumonia and Alzheimer's disease.
Pericyte physiology
Pericytes are cells that support blood vessels throughout the body. In the brain, these cells are able to contract, regulate brain blood flow and maintain the blood-brain barrier. In Alzheimer's disease, there is an early reduction in brain blood flow and increased blood-brain barrier permeability. We are studying brain pericyte physiology in health and disease. We seek to reveal whether they play a role in Alzheimer's disease pathophysiology.
Dementia in organoids
Alzheimer’s disease and related dementias impact the lives of millions of Americans, yet treatments are scarce and a cure does not exist. Although rodent studies have provided researchers insights into dementia pathogenesis, rodents without genetic modifications do not develop several hallmarks of Alzheimer’s disease, including β-Amyloid plaques and neurofibrillary tau tangles. Although there are efforts to humanize rodent models to model characteristics of human Alzheimer’s disease pathology, these models often fall short of recapitulating human-specific pathways. In addition, 99.6% of Alzheimer’s disease drugs that succeed in animal experiments fail in humans. Therefore, model systems that better recapitulate human-specific Alzheimer’s disease pathogenesis and biology are required.
The breakthrough of reprogramming donor somatic cells to human induced pluripotent stem (hiPS) cells and further differentiation into neural cell types has been instrumental in bridging this gap in research. In recent years, hiPS cells have been utilized in generating human brain organoids to study dementia pathology. These human brain organoids are three-dimensional structures containing functional neural circuits consisting of numerous subtypes of neuronal and glial cells. Although human brain organoids are typically used to study neurodevelopmental disorders as they are limited in their maturation, phenotypical differences relating to Alzheimer’s disease pathology have been observed in human brain organoid derived from hiPS cells reprogrammed from donors with Alzheimer’s disease.
Dementia biomarkers
The Nelson lab is measuring biomarkers in biofluids from intensive care unit patients with or without pneumonia, dementia patients, and healthy controls. Biomarkers of interest include tau (phophorylated and total), proinflammatory cytokines, neurofilament light chain, glial fibrillary acidic protein, and many others. Dr. Nelson has been using MesoScale Discovery for biomarker measurements for more than a decade and we are happy to have their latest plate reader in the lab.
Vascularizing human models
Dr. Nelson has a great interest in physiologically relevant human brain models with blood vessels and flow to use in the lab. Stay tuned for more updates as we embark on this new area of research.
Laboratory Collaborations
Nelson Lab current collaborators include:
Thomas Taylor-Clark, University of South Florida
Brant M. Wagener, University of Alabama at Birmingham
Anne Hiniker and Carol Church, University of Southern California
Zhen Zhao, Tulane University
Mike Lin and Troy Stevens, University of South Alabama
Corey E. Ventetuolo, Brown University