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.