Background: Sporadic Alzheimer’s Disease (AD) is assumed to be associated with different
biological/genetic vulnerability, as well as with neuroinflammation, mediated by cytokines. The present
study evaluated the role of cytokines in AD.
Objective: The aim was to determine the possible association of TNF-α (rs1800629), IL1-α (rs1800587)
and IL-10 (rs1800896) polymorphisms with AD, and to assess serum TNF-α, IL-1α and IL-10 concentrations
in patients with AD and in subjects with mild cognitive impairment (MCI).
Methods: The study included 645 Caucasian participants: 395 subjects with AD and 250 subjects with
MCI. Genotyping was performed using real-time PCR in all 645 subjects, while serum concentrations of
TNF-α, IL-1α and IL-10 and were determined using ELISA in 174 subjects.
Results: The frequency of the TNF-α rs1800629, IL1-α rs1800587 or IL-10 rs1800896 genotypes did
not differ significantly between patients with AD and MCI. Serum concentration of IL-1α and IL-10
were significantly decreased, while the concentration of TNF-α was significantly higher in patients with
AD than in MCI subjects. TNF-α, IL1-α or IL-10 concentrations were similar in subjects with AD or
MCI subdivided into carriers of the corresponding TNF-α rs1800629, IL1-α rs1800587 or IL-10
Conclusion: Similar distribution of the IL1-α rs1800587, TNF-α rs1800629 or IL-10 rs1800896 genotypes
in subjects with AD and MCI failed to confirm that these specific risk genotypes are associated
with vulnerability to develop AD. Alteration in IL-1α, IL-10 and TNF-α concentrations in patients with
AD partially confirmed the association with the neuroinflammatory response in AD.