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Cited by 117Neuroinflammation and Neurodegeneration MechanismsImmune Response and InflammationAnesthesia and Neurotoxicity Research

Toll-like receptor-mediated neuroinflammation: relevance for cognitive dysfunctions

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Squillace, Silvia, Salvemini, Daniela·2022·Trends in Pharmacological Sciences
DOI 10.1016/j.tips.2022.05.004PMC PMC9378500
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Abstract

Toll-like receptors (TLRs) are pattern recognition receptors (PRRs) with a well-documented role in the innate and adaptive immune responses. Interestingly, TLR activation has also been linked to several brain functions including neurogenesis and synaptogenesis. Increasing evidence supports TLR involvement in peripheral and central inflammation underlying normal aging and the pathogenesis of clinical conditions characterized by cognitive decline. These include not only major neurodegenerative diseases but also traumatic brain injuries, surgeries, and alcohol consumption- and chemotherapy-induced cognitive impairment. We first summarize the physiological roles of TLRs in the nervous system, and then illustrate the emerging involvement of TLRs in cognitive functions, pointing to these receptors as novel enticing pharmacological targets to develop more efficient drugs for the treatment of cognitive impairment.

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  • Systemic inflammation induced by activation of TLRs and inflammatory mediators such as TNFα causes cognitive decline and accelerates progression of Alzheimer's disease.

    “Systemic inflammation induced by the activation of Toll-like receptors (TLRs) and inflammatory mediators such as TNFα has been suggested to cause cognitive decline and accelerate the progression of Alzheimer’s disease (Squillace and Salvemini 2022; Holmes et al. 2009).”

    From Astrocyte-specific inhibition of the primary cilium suppresses C3 expression in reactive astrocyte (2024) · cites this paper as Squillace and Salvemini 2022

    The Alzheimer’s disease section says sustained TLR2 and TLR4 activation causes neuroinflammation and neurotoxic effects as disease progresses, supporting the suggested link to cognitive harm. It does not establish that systemic inflammation or TNFα accelerates Alzheimer’s progression; its explicit discussion of TNF release concerns Parkinson’s disease. The same Alzheimer’s section also describes protective effects of TLR activation in early disease and under mild stimulation. Page numbers are unavailable in our copy. (LLM, conf=0.85)

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Authors
Squillace, S., & Salvemini, D.
Affiliations
Saint Louis University (US)
Corresponding author
Salvemini, Daniela
ORCID
Venue
Trends in Pharmacological Sciences
Publisher
Elsevier BV
Published
2022-09
Volume
43
Issue
9
Pages
726-739
ISSN
0165-6147 (ISSN-L)
DOI
10.1016/j.tips.2022.05.004
PMC
PMC9378500
OpenAlex
W4283314958
Cited by
117
References
14
Citations by year
2026: 38 · 2025: 28 · 2024: 35 · 2023: 16
FWCI
2.02
Type
journal article
Language
en
Open access
Licence
Locations
  • Trends in Pharmacological Sciences (acceptedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institutes of Health (RO1CA230512, RO1NS111120)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Life Sciences › Neuroscience › Developmental Neuroscience › Anesthesia and Neurotoxicity Research
Keywords
Toll-like receptors, neuroinflammation, cognitive impairment, cognitive decline, neurodegenerative diseases, traumatic brain injury, alcohol-induced cognitive impairment, chemotherapy-induced cognitive impairment, neurogenesis, synaptogenesis, aging, therapeutic target
MeSH terms
Neuroinflammatory Diseases, Humans, Immunity, Innate, Inflammation, Neurodegenerative Diseases, Toll-Like Receptors, Cognitive Dysfunction

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