Microglial TLR4/NLRP3 Inflammasome Signaling in Alzheimer’s Disease

Dec 3, 2023Journal of Alzheimer's disease : JAD

Immune Cell Signaling Linked to Inflammation in Alzheimer's Disease

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Abstract

Approximately 70% of dementia cases worldwide are attributed to Alzheimer's disease.

The accumulation of amyloid-β and tau tangles, alongside neuroinflammation, are major pathological features of Alzheimer's disease.
Neuroinflammation is increasingly recognized as a significant area of research for Alzheimer's treatment.
Microglia, the primary immune cells in the central nervous system, play a crucial role in neuroinflammation associated with Alzheimer's disease.
Toll-like receptor 4 (TLR4) and NLRP3 inflammasomes are important molecules involved in neuroinflammation in Alzheimer's pathology.
The interaction between TLR4 and NLRP3 in microglia may influence the progression of Alzheimer's disease through neuroinflammatory mechanisms.
The potential of targeting TLR4 and NLRP3 as treatment options for Alzheimer's disease has been discussed.

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Alzheimer's disease is a pervasive neurodegenerative disease that is estimated to represent approximately 70% of dementia cases worldwide, and the molecular complexity that has been highlighted remains poorly understood. The accumulation of extracellular amyloid-β (Aβ), intracellular neurofibrillary tangles formed by tau hyperphosphorylation, and neuroinflammation are the major pathological features of Alzheimer's disease (AD). Over the years, there has been no apparent breakthrough in drug discovery based on the Aβ and tau hypotheses. Neuroinflammation has gradually become a hot spot in AD treatment research. As the primary cells of innate immunity in the central nervous system, microglia play a key role in neuroinflammation. Toll-like receptor 4 (TLR4) and nucleotide-binding oligomerization domain-like receptor 3 (NLRP3) inflammasomes are vital molecules in neuroinflammation. In the pathological context of AD, the complex interplay between TLR4 and the NLRP3 inflammasomes in microglia influences AD pathology via neuroinflammation. In this review, the effect of the activation and inhibition of TLR4 and NLRP3 in microglia on AD pathology, as well as the cross-talk between TLR4 and the NLRP3 inflammasome, and the influence of essential molecules in the relevant signaling pathway on AD pathology, were expounded. In addition, the feasibility of these factors in representing a potential treatment option for AD has been clarified.

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Microglial TLR4/NLRP3 Inflammasome Signaling in Alzheimer’s Disease

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