ReviewMolecular neurobiology2025
Central Role of Toll-like Receptor-9 Gene Function in Inflammation-Mediated Neuronal Plasticity: Implications for Long-Term Memory Development.
Review in Molecular neurobiology, 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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Authors and funding
4 authors.
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Abstract
Inflammation significantly influences various neurobiological processes, particularly in the context of the central nervous system (CNS). The Toll-like Receptor (TLR) 9 protein, a key component of the innate immune system, has been identified as a critical mediator of inflammatory responses in the CNS. This review explores the role of TLR9-mediated inflammatory responses in neuronal plasticity, focusing on long-term memory formation. A comprehensive literature review revealed that TLR9 activation instigates inflammatory responses in neurons, leading to the production of pro-inflammatory cytokines. These inflammatory responses, in turn, can induce DNA damage in neurons, which is integral to synaptic plasticity and memory formation. Activation of TLR9 promotes the expression of DNA repair proteins, facilitating the repair of DNA damage and ensuring neuronal survival. Disruption of TLR9 signaling impairs DNA repair and memory consolidation. The intricate interplay between TLR9, inflammation, and DNA damage plays a pivotal role in long-term memory formation, with potential implications for the pathophysiology of neurodegenerative disorders and memory enhancement strategies.
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Registered trials
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.