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, Stephane Hunot, Bertrand Joseph, Nikolaus Deigendesch, Olga Garaschuk, Erik Boddeke, Charles A. Dinarello, John C. Breitner, Greg M. Cole, Douglas T. Golenbock, Markus P. Kummer

*Bijbehorende auteur voor dit werk

Onderzoeksoutputpeer review

2255 Citaten (Scopus)


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.

Originele taal-2English
Pagina's (van-tot)388-405
Aantal pagina's18
TijdschriftLancet Neurology
Nummer van het tijdschrift4
StatusPublished - apr-2015

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