ReviewhLife2025
Mechanism of microglia-mediated neuroinflammation, associated cognitive dysfunction, and therapeutic updates in Alzheimer's disease.
Review in hLife, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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0 citing papers in PubMed.
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Authors and funding
7 authors.
Funding
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Abstract
Alzheimer's disease (AD) and associated cognitive dysfunction are major healthcare challenges globally. Various mechanisms of pathogenesis and signaling molecules have been studied for their plausible role in disease initiation and progression. Neuroinflammation has been considered a major hallmark of AD. Amyloid beta (Aβ), hyperphosphorylated tau protein, and formed neurofibrillary tangles (NFT) are positively correlated with neuroinflammation. Microglial activation was found to be a key contributor to neuroinflammation, AD pathogenesis, and progression. The mechanism of microglial activation has been studied in detail, and looking into its pivotal role in disease etiology, various drugs have been developed, and many are in the clinical phases of development. These drugs either inhibit the microglial activation or neuroinflammatory event postmicroglial activation. Considering these facts, in the present study, we herein discuss the mechanism of microglial activation and the mechanism of neuroinflammation related to microglial activation and dementia. Here we also discussed the various drugs that either act at tau protein or mitigate neuroinflammation, along with their status in clinical trials. In brief, this review provides an in-depth mechanism of microglial activation and updates on drugs that can inhibit this activation, leading to significant anti-Alzheimer effect and mitigation of cognitive dysfunction.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.