Abstract
Background: Alzheimer’s disease (AD) is the most common neurodegenerative disorder, neuropathologically characterized by aggregates of β-amyloid peptides, which deposit as senile plaques, and of TAU protein, which forms neurofibrillary tangles. It is now widely accepted that neuroinflammation is implicated in AD pathogenesis.
Method: Indeed, inflammatory mediators, such as cytokines and chemokines (chemotactic cytokines) can impact on the Alzheimer´s amyloid precursor protein by affecting its expression levels and amyloidogenic processing and/or β -amyloid aggregation. Additionally, cytokines and chemokines can influence kinases’ activities, leading to abnormal TAU phosphorylation. To date there is no cure for AD, but several therapeutic strategies have been directed to prevent neuroinflammation. Anti-inflammatory, but also anti-amyloidogenic compounds, such as flavonoids were shown to favourably modulate some pathological events associated with neurodegeneration. Conclusion: This review focuses on the role of cytokines and chemokines in AD-associated pathologies, and summarizes the potential anti-inflammatory therapeutic approaches aimed at preventing or slowing down disease progression.Keywords: Neuroinflammation, cytokines, chemokines, amyloid precursor protein, β-amyloid, TAU.
Current Alzheimer Research
Title:Impact of Cytokines and Chemokines on Alzheimer’s Disease Neuropathological Hallmarks
Volume: 14 Issue: 8
Author(s): Catarina Domingues, Odete A.B. da Cruz e Silva and Ana Gabriela Henriques*
Affiliation:
- Neurosciences and Signalling Laboratory, Department of Medical Sciences and Institute of Biomedicine - iBiMED, University of Aveiro, P.O. Box: 3810-193, Aveiro,Portugal
Keywords: Neuroinflammation, cytokines, chemokines, amyloid precursor protein, β-amyloid, TAU.
Abstract: Background: Alzheimer’s disease (AD) is the most common neurodegenerative disorder, neuropathologically characterized by aggregates of β-amyloid peptides, which deposit as senile plaques, and of TAU protein, which forms neurofibrillary tangles. It is now widely accepted that neuroinflammation is implicated in AD pathogenesis.
Method: Indeed, inflammatory mediators, such as cytokines and chemokines (chemotactic cytokines) can impact on the Alzheimer´s amyloid precursor protein by affecting its expression levels and amyloidogenic processing and/or β -amyloid aggregation. Additionally, cytokines and chemokines can influence kinases’ activities, leading to abnormal TAU phosphorylation. To date there is no cure for AD, but several therapeutic strategies have been directed to prevent neuroinflammation. Anti-inflammatory, but also anti-amyloidogenic compounds, such as flavonoids were shown to favourably modulate some pathological events associated with neurodegeneration. Conclusion: This review focuses on the role of cytokines and chemokines in AD-associated pathologies, and summarizes the potential anti-inflammatory therapeutic approaches aimed at preventing or slowing down disease progression.Export Options
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Cite this article as:
Domingues Catarina, da Cruz e Silva A.B. Odete and Henriques Gabriela Ana*, Impact of Cytokines and Chemokines on Alzheimer’s Disease Neuropathological Hallmarks, Current Alzheimer Research 2017; 14 (8) . https://dx.doi.org/10.2174/1567205014666170317113606
DOI https://dx.doi.org/10.2174/1567205014666170317113606 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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