IL_33 as a Modulator of Neuroinflammation in Alzheimer’s disease: An ELISA Approach

Abstract

Alzheimer’s disease (AD) is a devastating condition with no known effective treatment. AD is characterized by memory loss as well as impaired locomotor ability, reasoning, and judgment. Emerging evidence suggests that the innate immune response plays a major role in the pathogenesis of AD. In AD, the accumulation of β-amyloid (Aβ) in the brain perturbs physiological functions of the brain, including synaptic and neuronal dysfunction, microglial activation, and neuronal loss. Serum levels of soluble ST2 (sST2), a decoy receptor for interleukin (IL)-33, increase in patients with mild cognitive impairment, suggesting that impaired IL-33/ST2 signaling may contribute to the pathogenesis of AD. Therefore, we investigated the potential therapeutic role of IL-33 in AD. Our results demonstrate a potential therapeutic role for IL-33 in AD. The elevated levels of IL-33 in Alzheimer’s disease patients highlight a promising area of research that could have significant implications for the understanding and management of the disease.