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TLR2 and TLR4-mediated inflammation in Alzheimer`s disease: self-defense or sabotage?

Dallas, M. ORCID: https://orcid.org/0000-0002-5190-0522 and Widera, D. ORCID: https://orcid.org/0000-0003-1686-130X (2020) TLR2 and TLR4-mediated inflammation in Alzheimer`s disease: self-defense or sabotage? Neural Regeneration Research. ISSN 1876-7958 (In Press)

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Abstract/Summary

In summary, the research field of inflammation is rapidly expanding in the milieu of neurodegenerative diseases. The current evidence presents snapshots in time of the cellular players and their production of inflammatory biomarkers. This is an underestimation of the complexities of inflammatory processes within the brain involved in development and progression of neurodegenerative disorders that might have resulted in the failure of NSAID based prevention and treatment strategies in AD. We postulate that inflammation has an intrinsically dual role in AD. In the acute phase, TLR2 and TLR4-mediated inflammation in the brain represents a self-defence mechanism which affords protection. Therefore, a global inhibition of inflammatory signalling as a preventive measure during the acute phase might not be only ineffective but could even counteract regenerative processes. In contrast, uncontrolled and continuous high levels of inflammation resulting from the feed-forward inflammatory loop mediated by TLR2 and TLR4 are neurodegenerative and causative in the disease progression. Together this creates a therapeutic window aiming to prevent the switch from the acute to the chronic phase before AD clinical presentation to slow down disease progression. The challenge for the Alzheimer’s research community now will be to accurately identify this window in a clinically relevant patient population.

Item Type:Article
Refereed:Yes
Divisions:Interdisciplinary centres and themes > Centre for Integrative Neuroscience and Neurodynamics (CINN)
Faculty of Life Sciences > School of Chemistry, Food and Pharmacy > School of Pharmacy > Division of Pharmacology
ID Code:93569
Publisher:Wolters Kluwer

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