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The present review describes the modulatory role of the TLR signaling pathway in the inflammatory responses developed following various CVDs and discusses the potential benefits of the modulation of different TLRs in the improvement of functional outcomes after brain ischemia.
TLRs are involved in the development and progression of neuroimmune diseases via initiating inflammatory responses. Thus, targeting TLRs signaling pathway may be considered as a potential therapy for neuroimmune diseases. However, the role of TLRs is elusive and complex in neuroimmune diseases.
As the TLR-4 signaling pathway is involved in the neuroinflammation process in various NDDs such as AD, PD, HD, stroke, and ALS, in this review we summarise the various TLR-4/NF-κB inhibitors which appear to be most studied for neuroprotection.
Toll-like receptors (TLRs) shape trained immunity, balancing infection responses and chronic inflammation, and TLR agonists are promising immunomodulators for infectious diseases and cancer.
Here, we review current data regarding the pathophysiological role of TLR signaling pathways in different CVDs and discuss the role of SD in the potentiation of the inflammatory cascade in CVDs through the modulation of TLRs.
Different stressors can elicit neuroinflammatory responses modulated by innate immunity receptors, such as the family of Toll-like receptors (TLRs). The TLR4, a pattern recognition receptor (PRR), is involved in many diseases, such as inflammatory and central nervous system (CNS) diseases.
In this review, we summarize the key evidence supporting TLR4 as a promising therapeutic target in AD treatment. Alzheimer disease (AD) is a progressive and irreversible neurodegenerative disease that mainly manifests as memory loss and cognitive deterioration.
In this review article, we focus on the TLR family and their respective ligands, structures, and signaling pathways and also point at the role of TLRs in ischemic stroke emphasizing the interaction with neurosteroids.
This study is focused on the potential roles of various TLRs in various neurodegenerative diseases such as Parkinson’s disease (PD) and Alzheimer’s disease (AD), namely TLR2, TLR3, TLR4, TLR7, and TLR9 in AD and PD in human beings and a mouse model. 1. Introduction.
Activation of neuronal TLR3, TLR7 and TLR8 with nucleic acids negatively modulates neurite outgrowth and alters synapse formation in a cell-autonomous manner. It consequently influences neural connectivity and brain function and leads to deficits related to neuropsychiatric disorders.