Year: 2022
Type: article
Abstract: Neuroinflammation has been recognized as a component of Alzheimer's Disease (AD) pathology since the original descriptions by Alois Alzheimer and a role for infections in AD pathogenesis has long been hypothesized. More recently, this hypothesis has gained strength as human genetics and experimental data suggest key roles for inflammatory cells in AD pathogenesis. To review this topic, Duke/University of North Carolina (Duke/UNC) Alzheimer's Disease Research Center hosted a virtual symposium: "Infection and Inflammation: New Perspectives on Alzheimer's Disease (AD)." Participants considered current evidence for and against the hypothesis that AD could be caused or exacerbated by infection or commensal microbes. Discussion focused on connecting microglial transcriptional states to functional states, mouse models that better mimic human immunity, the potential involvement of inflammasome signaling, metabolic alterations, self-reactive T cells, gut microbes and fungal infections, and lessons learned from Covid-19 patients with neurologic symptoms. The content presented in the symposium, and major topics raised in discussions are reviewed in this summary of the proceedings.
Authors: Heather E. Whitson, Carol Colton, Joseph El Khoury, David Gate, Alison Goate, Michael T. Heneka, Rima Kaddurah-Daouk, Robyn S. Klein, Mari L. Shinohara, Sangram Sisodia, Serena S. Spudich, Beth Stevens, Rudolph Tanzi, Jenny P. Ting, Gwenn Garden, Alison Aiello, Ornit Chiba-Falek, Joseph Heitman, Kim G. Johnson, Micah Luftig, Ashley Moseman, Jonathan Rawls, Mari L. Shinohara, Ronald Swanstrom, Niccolo Terrando
Institutions: Duke University, Duke Medical Center, Durham VA Medical Center, Massachusetts General Hospital, Northwestern University, Icahn School of Medicine at Mount Sinai, University of Bonn, Washington University in St. Louis, University of Chicago, Yale University, Boston Children's Hospital, University of North Carolina at Chapel Hill, UNC Lineberger Comprehensive Cancer Center
Language: English
Subfield: Neurology
Field: Neuroscience
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $2,500
Funders: National Multiple Sclerosis Society, Biogen, Cure Alzheimer's Fund, Open Philanthropy Project, IFM Therapeutics, Shijiazhuang Tiedao University, Multiple Sclerosis Society, National Institutes of Health, National Institute on Aging, National Institute of Allergy and Infectious Diseases, National Institute of Neurological Disorders and Stroke, National Center for Advancing Translational Sciences
Awards: G1044130170, G104586243, Genomic approach to identification of microglial networks involved in Alzheimer disease risk, G1249643857, Metabolic Networks and Pathways Predictive of Sex Differences in AD Risk and Responsiveness to Treatment, G1567426788, G160496021, G1625759367, G1665691986, Metabolic Network Analysis of Biochemical Trajectories in Alzheimer's Disease, G1700269184, G1814223534, G2149305019, G2234397790, G238180650, G2448835408, G2777672791, G3045628926, G3146424788, G3359879711, Sex and APOE genotype interact to alter immune regulated metabolism in AD, Gut Liver Brain Biochemical Axis in Alzheimer's Disease, G417899861, G4255341093, Metabolic Signatures Underlying Vascular Risk Factors for Alzheimer-type Dementias, G4973850323, G5190695102, G5293636047, G5679185021, G5993441859, G6371410416, G6672412616, Metabolic Networks and Pathways in Alzheimer's Disease, G9000067356, G9000074613, G9000091371, G9000122335, G9000124253, G9000168410, G9000183971, G9000206009, G9000302701, G9000308166, Molecular and Functional Analysis of Innate Immune Receptors
OpenAlex ID: W4224264144