ArticleACS chemical neuroscience2025
Intraventricular Creatine Treatment Attenuates Alzheimer's Disease-Related Neuropathological Changes and Memory Impairment via Inhibiting STAT1 Phosphorylation.
Article in ACS chemical neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Interferon-induced protein IFIT3 as a molecular nexus of neuroinflammation in Alzheimer's disease and HIV-associated neurocognitive disorders.Journal of neuroinflammation · 2026Article
- MALT1 in cerebrospinal fluid: a prognostic biomarker and potential therapeutic target in Alzheimer's disease.Frontiers in neurology · 2025Article
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12 authors.
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Abstract
The importance of neuroinflammation in Alzheimer's disease (AD) has attracted increasing attention, and the functions of the STAT1 signaling pathway have also generated widespread interest. However, the role of STAT1 in AD-related neuroinflammation and memory impairment is unclear. Therefore, this study was undertaken to elucidate the roles of the STAT1 signaling pathway in the brain tissue of AD patients and mouse of an AD model. Our results revealed that STAT1 phosphorylation was largely colocalized with the neuronal marker NeuN. Compared with that in control (non-AD) brain tissues, STAT1 phosphorylation was significantly upregulated in the brain cortex and hippocampus of both AD patients and FAD mice. Intraventricular injection of creatine (STAT1 signaling inhibitor) significantly reduced the level of neuronal STAT1 phosphorylation in the brain cortex and markedly alleviated cognitive impairment in FAD mice. Furthermore, intraventricular creatine treatment also reduced the number of Aβ plaques and the level of IBA1 expression in IBA1-positive microglia in FAD mice. These findings indicate that STAT1 phosphorylation may play an important role in AD-related neuroinflammation and memory impairment. The alleviation effects of intraventricular creatine in FAD mice may suggest that STAT1 is a potential therapeutic target for the treatment of AD in humans.
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