Infection and inflammation: New perspectives on Alzheimer's disease

Symposium Planning Committee members

doi:10.1016/j.bbih.2022.100462

Infection and inflammation: New perspectives on Alzheimer's disease

Symposium Planning Committee members

Neurology

Research output: Contribution to journal › Review article › peer-review

21 Scopus citations

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.

Original language	English (US)
Article number	100462
Journal	Brain, Behavior, and Immunity - Health
Volume	22
DOIs	https://doi.org/10.1016/j.bbih.2022.100462
State	Published - Jul 2022

Keywords

Alzheimer's
Fungi
Infection
Inflammasome
Inflammation
Metabolism
Microbe
Microbiome
Microglia

ASJC Scopus subject areas

Nephrology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.bbih.2022.100462

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@article{d732406c1282419cb92f1425581f5630,

title = "Infection and inflammation: New perspectives on Alzheimer's disease",

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.",

keywords = "Alzheimer's, Fungi, Infection, Inflammasome, Inflammation, Metabolism, Microbe, Microbiome, Microglia",

author = "{Symposium Planning Committee members} and Whitson, {Heather E.} and Carol Colton and {El Khoury}, Joseph and David Gate and Alison Goate and Heneka, {Michael T.} and Rima Kaddurah-Daouk and Klein, {Robyn S.} and Shinohara, {Mari L.} and Sangram Sisodia and Spudich, {Serena S.} and Beth Stevens and Rudolph Tanzi and Ting, {Jenny P.} and Gwenn Garden and Alison Aiello and Ornit Chiba-Falek and Joseph Heitman and Johnson, {Kim G.} and Micah Luftig and Ashley Moseman and Jonathan Rawls and Ronald Swanstrom and Niccolo Terrando",

note = "Publisher Copyright: {\textcopyright} 2022",

year = "2022",

month = jul,

doi = "10.1016/j.bbih.2022.100462",

language = "English (US)",

volume = "22",

journal = "Brain, Behavior, and Immunity - Health",

issn = "2666-3546",

publisher = "Elsevier Inc.",

}

TY - JOUR

T1 - Infection and inflammation

T2 - New perspectives on Alzheimer's disease

AU - Symposium Planning Committee members

AU - Whitson, Heather E.

AU - Colton, Carol

AU - El Khoury, Joseph

AU - Gate, David

AU - Goate, Alison

AU - Heneka, Michael T.

AU - Kaddurah-Daouk, Rima

AU - Klein, Robyn S.

AU - Shinohara, Mari L.

AU - Sisodia, Sangram

AU - Spudich, Serena S.

AU - Stevens, Beth

AU - Tanzi, Rudolph

AU - Ting, Jenny P.

AU - Garden, Gwenn

AU - Aiello, Alison

AU - Chiba-Falek, Ornit

AU - Heitman, Joseph

AU - Johnson, Kim G.

AU - Luftig, Micah

AU - Moseman, Ashley

AU - Rawls, Jonathan

AU - Swanstrom, Ronald

AU - Terrando, Niccolo

PY - 2022/7

Y1 - 2022/7

N2 - 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.

AB - 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.

KW - Alzheimer's

KW - Fungi

KW - Infection

KW - Inflammasome

KW - Inflammation

KW - Metabolism

KW - Microbe

KW - Microbiome

KW - Microglia

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U2 - 10.1016/j.bbih.2022.100462

DO - 10.1016/j.bbih.2022.100462

M3 - Review article

C2 - 36118272

AN - SCOPUS:85133316061

SN - 2666-3546

VL - 22

JO - Brain, Behavior, and Immunity - Health

JF - Brain, Behavior, and Immunity - Health

M1 - 100462

ER -

Infection and inflammation: New perspectives on Alzheimer's disease

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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