Neuroinflammation in Alzheimer's disease

Michael T Heneka; Monica J Carson; Joseph El Khoury; Gary E Landreth; Frederic Brosseron; Douglas L Feinstein; Andreas H Jacobs; Tony Wyss-Coray; Javier Vitorica; Richard M Ransohoff; Karl Herrup; Sally A Frautschy; Bente Finsen; Guy C Brown; Alexei Verkhratsky; Koji Yamanaka; Jari Koistinaho; Eicke Latz; Annett Halle; Gabor C Petzold; Terrence Town; Dave Morgan; Mari L Shinohara; V Hugh Perry; Clive Holmes; Nicolas G Bazan; David J Brooks; Stéphane Hunot; Bertrand Joseph; Nikolaus Deigendesch; Olga Garaschuk; Erik Boddeke; Charles A Dinarello; John C Breitner; Greg M Cole; Douglas T Golenbock; Markus P Kummer

doi:10.1016/S1474-4422(15)70016-5

Neuroinflammation in Alzheimer's disease

Michael T Heneka, Monica J Carson, Joseph El Khoury, Gary E Landreth, Frederic Brosseron, Douglas L Feinstein, Andreas H Jacobs, Tony Wyss-Coray, Javier Vitorica, Richard M Ransohoff, Karl Herrup, Sally A Frautschy, Bente Finsen, Guy C Brown, Alexei Verkhratsky, Koji Yamanaka, Jari Koistinaho, Eicke Latz, Annett Halle, Gabor C PetzoldTerrence Town, Dave Morgan, Mari L Shinohara, V Hugh Perry, Clive Holmes, Nicolas G Bazan, David J Brooks, Stéphane Hunot, Bertrand Joseph, Nikolaus Deigendesch, Olga Garaschuk, Erik Boddeke, Charles A Dinarello, John C Breitner, Greg M Cole, Douglas T Golenbock, Markus P Kummer

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

Abstrakt

Increasing evidence suggests that Alzheimer's disease pathogenesis is not restricted to the neuronal compartment, but includes strong interactions with immunological mechanisms in the brain. Misfolded and aggregated proteins bind to pattern recognition receptors on microglia and astroglia, and trigger an innate immune response characterised by release of inflammatory mediators, which contribute to disease progression and severity. Genome-wide analysis suggests that several genes that increase the risk for sporadic Alzheimer's disease encode factors that regulate glial clearance of misfolded proteins and the inflammatory reaction. External factors, including systemic inflammation and obesity, are likely to interfere with immunological processes of the brain and further promote disease progression. Modulation of risk factors and targeting of these immune mechanisms could lead to future therapeutic or preventive strategies for Alzheimer's disease.

Originalsprog	Engelsk
Tidsskrift	Lancet Neurology
Vol/bind	14
Udgave nummer	4
Sider (fra-til)	388-405
Antal sider	18
ISSN	1474-4422
DOI	https://doi.org/10.1016/S1474-4422(15)70016-5
Status	Udgivet - 1. apr. 2015

Dokumenter og links

10.1016/S1474-4422(15)70016-5

Citationsformater

Heneka, M. T., Carson, M. J., Khoury, J. E., Landreth, G. E., Brosseron, F., Feinstein, D. L., Jacobs, A. H., Wyss-Coray, T., Vitorica, J., Ransohoff, R. M., Herrup, K., Frautschy, S. A., Finsen, B., Brown, G. C., Verkhratsky, A., Yamanaka, K., Koistinaho, J., Latz, E., Halle, A., ... Kummer, M. P. (2015). Neuroinflammation in Alzheimer's disease. Lancet Neurology, 14(4), 388-405. https://doi.org/10.1016/S1474-4422(15)70016-5

@article{42864436fc1a46c090b10bafce5f3244,

title = "Neuroinflammation in Alzheimer's disease",

abstract = "Increasing evidence suggests that Alzheimer's disease pathogenesis is not restricted to the neuronal compartment, but includes strong interactions with immunological mechanisms in the brain. Misfolded and aggregated proteins bind to pattern recognition receptors on microglia and astroglia, and trigger an innate immune response characterised by release of inflammatory mediators, which contribute to disease progression and severity. Genome-wide analysis suggests that several genes that increase the risk for sporadic Alzheimer's disease encode factors that regulate glial clearance of misfolded proteins and the inflammatory reaction. External factors, including systemic inflammation and obesity, are likely to interfere with immunological processes of the brain and further promote disease progression. Modulation of risk factors and targeting of these immune mechanisms could lead to future therapeutic or preventive strategies for Alzheimer's disease.",

keywords = "Alzheimer Disease/genetics, Animals, Anti-Inflammatory Agents, Non-Steroidal/therapeutic use, Astrocytes/immunology, Biomarkers/blood, Brain Injuries/complications, Clinical Trials as Topic, Disease Models, Animal, Disease Progression, Humans, Immunity, Innate, Immunization, Inflammation Mediators/immunology, Inflammation/diagnosis, Locus Coeruleus/pathology, Microglia/immunology, Nootropic Agents/administration & dosage, Obesity/complications, Phagocytosis, Protein Folding, Risk Factors, Severity of Illness Index",

author = "Heneka, {Michael T} and Carson, {Monica J} and Khoury, {Joseph El} and Landreth, {Gary E} and Frederic Brosseron and Feinstein, {Douglas L} and Jacobs, {Andreas H} and Tony Wyss-Coray and Javier Vitorica and Ransohoff, {Richard M} and Karl Herrup and Frautschy, {Sally A} and Bente Finsen and Brown, {Guy C} and Alexei Verkhratsky and Koji Yamanaka and Jari Koistinaho and Eicke Latz and Annett Halle and Petzold, {Gabor C} and Terrence Town and Dave Morgan and Shinohara, {Mari L} and Perry, {V Hugh} and Clive Holmes and Bazan, {Nicolas G} and Brooks, {David J} and St{\'e}phane Hunot and Bertrand Joseph and Nikolaus Deigendesch and Olga Garaschuk and Erik Boddeke and Dinarello, {Charles A} and Breitner, {John C} and Cole, {Greg M} and Golenbock, {Douglas T} and Kummer, {Markus P}",

year = "2015",

month = apr,

day = "1",

doi = "10.1016/S1474-4422(15)70016-5",

language = "English",

volume = "14",

pages = "388--405",

journal = "Lancet Neurology",

issn = "1474-4422",

publisher = "TheLancet Publishing Group",

number = "4",

}

Heneka, MT, Carson, MJ, Khoury, JE, Landreth, GE, Brosseron, F, Feinstein, DL, Jacobs, AH, Wyss-Coray, T, Vitorica, J, Ransohoff, RM, Herrup, K, Frautschy, SA, Finsen, B, Brown, GC, Verkhratsky, A, Yamanaka, K, Koistinaho, J, Latz, E, Halle, A, Petzold, GC, Town, T, Morgan, D, Shinohara, ML, Perry, VH, Holmes, C, Bazan, NG, Brooks, DJ, Hunot, S, Joseph, B, Deigendesch, N, Garaschuk, O, Boddeke, E, Dinarello, CA, Breitner, JC, Cole, GM, Golenbock, DT & Kummer, MP 2015, 'Neuroinflammation in Alzheimer's disease', Lancet Neurology, bind 14, nr. 4, s. 388-405. https://doi.org/10.1016/S1474-4422(15)70016-5

TY - JOUR

T1 - Neuroinflammation in Alzheimer's disease

AU - Heneka, Michael T

AU - Carson, Monica J

AU - Khoury, Joseph El

AU - Landreth, Gary E

AU - Brosseron, Frederic

AU - Feinstein, Douglas L

AU - Jacobs, Andreas H

AU - Wyss-Coray, Tony

AU - Vitorica, Javier

AU - Ransohoff, Richard M

AU - Herrup, Karl

AU - Frautschy, Sally A

AU - Finsen, Bente

AU - Brown, Guy C

AU - Verkhratsky, Alexei

AU - Yamanaka, Koji

AU - Koistinaho, Jari

AU - Latz, Eicke

AU - Halle, Annett

AU - Petzold, Gabor C

AU - Town, Terrence

AU - Morgan, Dave

AU - Shinohara, Mari L

AU - Perry, V Hugh

AU - Holmes, Clive

AU - Bazan, Nicolas G

AU - Brooks, David J

AU - Hunot, Stéphane

AU - Joseph, Bertrand

AU - Deigendesch, Nikolaus

AU - Garaschuk, Olga

AU - Boddeke, Erik

AU - Dinarello, Charles A

AU - Breitner, John C

AU - Cole, Greg M

AU - Golenbock, Douglas T

AU - Kummer, Markus P

PY - 2015/4/1

Y1 - 2015/4/1

N2 - Increasing evidence suggests that Alzheimer's disease pathogenesis is not restricted to the neuronal compartment, but includes strong interactions with immunological mechanisms in the brain. Misfolded and aggregated proteins bind to pattern recognition receptors on microglia and astroglia, and trigger an innate immune response characterised by release of inflammatory mediators, which contribute to disease progression and severity. Genome-wide analysis suggests that several genes that increase the risk for sporadic Alzheimer's disease encode factors that regulate glial clearance of misfolded proteins and the inflammatory reaction. External factors, including systemic inflammation and obesity, are likely to interfere with immunological processes of the brain and further promote disease progression. Modulation of risk factors and targeting of these immune mechanisms could lead to future therapeutic or preventive strategies for Alzheimer's disease.

AB - Increasing evidence suggests that Alzheimer's disease pathogenesis is not restricted to the neuronal compartment, but includes strong interactions with immunological mechanisms in the brain. Misfolded and aggregated proteins bind to pattern recognition receptors on microglia and astroglia, and trigger an innate immune response characterised by release of inflammatory mediators, which contribute to disease progression and severity. Genome-wide analysis suggests that several genes that increase the risk for sporadic Alzheimer's disease encode factors that regulate glial clearance of misfolded proteins and the inflammatory reaction. External factors, including systemic inflammation and obesity, are likely to interfere with immunological processes of the brain and further promote disease progression. Modulation of risk factors and targeting of these immune mechanisms could lead to future therapeutic or preventive strategies for Alzheimer's disease.

KW - Alzheimer Disease/genetics

KW - Animals

KW - Anti-Inflammatory Agents, Non-Steroidal/therapeutic use

KW - Astrocytes/immunology

KW - Biomarkers/blood

KW - Brain Injuries/complications

KW - Clinical Trials as Topic

KW - Disease Models, Animal

KW - Disease Progression

KW - Humans

KW - Immunity, Innate

KW - Immunization

KW - Inflammation Mediators/immunology

KW - Inflammation/diagnosis

KW - Locus Coeruleus/pathology

KW - Microglia/immunology

KW - Nootropic Agents/administration & dosage

KW - Obesity/complications

KW - Phagocytosis

KW - Protein Folding

KW - Risk Factors

KW - Severity of Illness Index

U2 - 10.1016/S1474-4422(15)70016-5

DO - 10.1016/S1474-4422(15)70016-5

M3 - Journal article

C2 - 25792098

VL - 14

SP - 388

EP - 405

JO - Lancet Neurology

JF - Lancet Neurology

SN - 1474-4422

IS - 4

ER -

Neuroinflammation in Alzheimer's disease

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