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Targeting Neuroinflammation to Treat Alzheimer’s Disease

Ardura-Fabregat, A.; Boddeke, E. W.G.M.; Boza-Serrano, A. LU ; Brioschi, S.; Castro-Gomez, S.; Ceyzériat, K.; Dansokho, C.; Dierkes, T.; Gelders, G. and Heneka, Michael T., et al. (2017) In CNS Drugs 31(12). p.1-26
Abstract

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... (More)

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.

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@article{342294cd-fa55-4327-abb7-fc1e2d56fbd4,
  abstract     = {<p>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.</p>},
  author       = {Ardura-Fabregat, A. and Boddeke, E. W.G.M. and Boza-Serrano, A. and Brioschi, S. and Castro-Gomez, S. and Ceyzériat, K. and Dansokho, C. and Dierkes, T. and Gelders, G. and Heneka, Michael T. and Hoeijmakers, L. and Hoffmann, A. and Iaccarino, L. and Jahnert, S. and Kuhbandner, K. and Landreth, G. and Lonnemann, N. and Löschmann, P. A. and McManus, R. M. and Paulus, A. and Reemst, K. and Sanchez-Caro, J. M. and Tiberi, A. and van der Perren, A. and Vautheny, A. and Venegas, C. and Webers, A. and Weydt, P. and Wijasa, T. S. and Xiang, X. and Yang, Y.},
  issn         = {1172-7047},
  language     = {eng},
  month        = {12},
  number       = {12},
  pages        = {1--26},
  publisher    = {Adis International},
  series       = {CNS Drugs},
  title        = {Targeting Neuroinflammation to Treat Alzheimer’s Disease},
  url          = {http://dx.doi.org/10.1007/s40263-017-0483-3},
  volume       = {31},
  year         = {2017},
}