Targeting Neuroinflammation to Treat Alzheimer's Disease

A. Ardura-Fabregat, E. W. G. M. Boddeke, A. Boza-Serrano, S. Brioschi, S. Castro-Gomez, K. Ceyzeriat, C. Dansokho, T. Dierkes, G. Gelders, Michael T. Heneka*, L. Hoeijmakers, A. Hoffmann, L. Iaccarino, S. Jahnert, K. Kuhbandner, G. Landreth, N. Lonnemann, P. A. Loeschmann, R. M. McManus, A. PaulusK. Reemst, J. M. Sanchez-Caro, A. Tiberi, A. Van der Perren, A. Vautheny, C. Venegas, A. Webers, P. Weydt, T. S. Wijasa, X. Xiang, Y. Yang

*Bijbehorende auteur voor dit werk

Onderzoeksoutputpeer review

98 Citaten (Scopus)
345 Downloads (Pure)


Over the past few decades, research on Alzheimer's disease (AD) has focused on pathomechanisms linked to two of the major pathological hallmarks of extracellular deposition of beta-amyloid peptides and intra-neuronal formation of neurofibrils. Recently, a third disease component, the neuroinflammatory reaction mediated by cerebral innate immune cells, has entered the spotlight, prompted by findings from genetic, pre-clinical, and clinical studies. Various proteins that arise during neurodegeneration, including beta-amyloid, tau, heat shock proteins, and chromogranin, among others, act as danger-associated molecular patterns, that-upon engagement of pattern recognition receptors-induce inflammatory signaling pathways and ultimately lead to the production and release of immune mediators. These may have beneficial effects but ultimately compromise neuronal function and cause cell death. The current review, assembled by participants of the Chiclana Summer School on Neuroinflammation 2016, provides an overview of our current understanding of AD-related immune processes. We describe the principal cellular and molecular players in inflammation as they pertain to AD, examine modifying factors, and discuss potential future therapeutic targets.

Originele taal-2English
Pagina's (van-tot)1057-1082
Aantal pagina's26
TijdschriftCns Drugs
Nummer van het tijdschrift12
StatusPublished - dec-2017

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