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Targeting Neuroinflammation to Treat Alzheimer's Disease

Ardura-Fabregat, A., Boddeke, E. W. G. M., Boza-Serrano, A., Brioschi, S., Castro-Gomez, S., Ceyzeriat, K., Dansokho, C., Dierkes, T., Gelders, G., Heneka, M. T., Hoeijmakers, L., Hoffmann, A., Iaccarino, L., Jahnert, S., Kuhbandner, K., Landreth, G., Lonnemann, N., Loeschmann, P. A., McManus, R. M., Paulus, A., Reemst, K., Sanchez-Caro, J. M., Tiberi, A., Van der Perren, A., Vautheny, A., Venegas, C., Webers, A., Weydt, P., Wijasa, T. S., Xiang, X. & Yang, Y., Dec-2017, In : Cns Drugs. 31, 12, p. 1057-1082 26 p.

Research output: Contribution to journalReview articleAcademicpeer-review

  • 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. Paulus
  • K. 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

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.

Original languageEnglish
Pages (from-to)1057-1082
Number of pages26
JournalCns Drugs
Volume31
Issue number12
Publication statusPublished - Dec-2017

    Keywords

  • MILD COGNITIVE IMPAIRMENT, POSITRON-EMISSION-TOMOGRAPHY, ANTIINFLAMMATORY PREVENTION TRIAL, TRAUMATIC BRAIN-INJURY, HERPES-SIMPLEX-VIRUS, AMYLOID-BETA-PEPTIDE, RANDOMIZED CONTROLLED-TRIAL, PERIPHERAL BENZODIAZEPINE-RECEPTOR, ADULT HIPPOCAMPAL NEUROGENESIS, INDUCED MICROGLIAL ACTIVATION

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