Background: Growing body of evidence suggests that the pathogenesis of Alzheimer’s
disease (AD), a progressing neurodegenerative condition, is not limited to the neuronal compartment,
but also involves various immunological mechanisms. Insoluble Aβ aggregates in the brain can
induce the activation of microglia, resulting in the synthesis of proinflammatory mediators, which
further can stimulate astrocytic expression of YKL-40. Therefore, the aim of the current review is to
present up-to-date data about the role of YKL-40 as a biomarker of AD as well as the possibility of
therapeutic strategies targeting neuroinflammation.
Objective/Methods: We searched PubMed articles for the terms “YKL-40”, “neurodegeneration”,
“neuroinflammation” and “Alzheimer’s disease”, and included papers focusing on this review’s scope.
Results: Recent studies indicate that CSF concentrations of YKL-40 were significantly higher in AD
patients than in cognitively normal individuals and correlated with dementia biomarkers, such as tau
proteins and amyloid beta. Determination of YKL-40 CSF concentration may be also helpful in
differentiation between types of dementia and in the distinction of patients in the stable phase of MCI
from those who progressed to dementia. Moreover, significantly increased levels of YKL-40 mRNA
were found in AD brains in comparison with non-demented controls. Additionally, it was suggested
that anti-inflammatory treatment might relief the symptoms of AD and slow its progression.
Conclusion: Based on the recent knowledge, YKL-40 might be useful as a possible biomarker in the
diagnosis and prognosis of AD. Modulation of risk factors and targeting of immune mechanisms,
including systemic inflammation could lead to future preventive or therapeutic strategies for AD.