Volume 30, Issue 174, August 2026

Neuroinflammation in Alzheimer’s disease: current evidence and therapeutic targets

Jan Olszewski^♦, Szymon Uszak, Julia Rojek, Patrycja Jędrzejewska, Tomasz Szczawiński, Izabela Ślusarczyk, Wojciech Szlajss, Daria Wieczorek, Natalia Kruk, Adrianna Chachuła

Medical University of Lodz: Lodz, Łódź Voivodeship, Poland

^♦Corresponding author
Jan Olszewski, Medical University of Lodz: Lodz, Łódź Voivodeship, Poland

ABSTRACT

Background/Purpose: A key part of what causes Alzheimer's disease (AD) is inflammation in the brain. In the past, this was seen as a result of other problems, but now we know that it's a main cause of brain cell damage. This review synthesizes current evidence on about the molecular mechanisms, cellular mediators, and therapeutic strategies that target neuroinflammation in AD. Methods: We searched for information using these keywords: neuroinflammation and Alzheimer's disease, microglia in AD, the NLRP3 inflammasome and neurodegeneration, TREM2 in AD, astrocytes and neuroinflammation, the bloodbrain barrier in AD, the JAK/STAT pathway and neuroinflammation, and GLP-1 receptor agonists and neurodegeneration. The publication date was the most important factor for articles published between 2022 and 2026. Findings: In Alzheimer's disease (AD), two types of cells, microglia and astrocytes, play a key role in causing the inflammation of the brain. This imbalance drives the accumulation of amyloid-beta (Aβ) and promotes abnormal tau hyperactivity. The NLRP3 inflammasome, NF-κB, and JAK/STAT pathways are the main molecular mediators of chronic neuroinflammatory signaling. Therapeutic strategies targeting TREM2, IL-1β/IL-18, GLP-1 receptors, Nrf2, and natural compounds show promise in preclinical and early clinical trials. The blood-brain barrier and immune cell infiltration are important to understand for the treatment of neuroinflammation. Conclusion: By synthesizing evidence published between January 2022 and March 2026, this review provides a comprehensive account of the mechanisms underlying neuroinflammation in Alzheimer's disease. These mechanisms are similar to current investigational therapeutic agents, such as small-molecule agonists in Phase 2 clinical trials.

Keywords: Alzheimer’s disease, neuroinflammation, microglia, NLRP3 inflammasome, TREM2, therapeutic targets.

Medical Science, 2026, 30, e168ms3927

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DOI: https://doi.org/10.54905/disssi.v30i174.e168ms3927

Published: 27 August 2026