Abstract
Toll-like receptors (TLRs) are important innate immune proteins, and the activation of the TLRs results in the activation of intracellular signaling pathways, leading to the expression of proinflammatory cytokines that are essential to the identification and clearance of invading pathogens. TLR signaling occurs through adaptor proteins, most commonly myeloid differentiation primary response gene 88 (MyD88). It is now known that immune surveillance and inflammatory responses occur in neurodegenerative diseases and TLR/MYD88 signaling plays a critical role in these diseases. The included studies suggest a contribution for this signaling to the pathophysiology of Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, multiple system atrophy, and related disorders. In this review, a discussion of the recent findings in this field is presented.
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©2015 by De Gruyter
Articles in the same Issue
- Frontmatter
- Neuroprotective effects of geniposide on Alzheimer’s disease pathology
- Autophagy in Alzheimer’s disease
- Spinal cord injury: overview of experimental approaches used to restore locomotor activity
- Role of Toll-like receptor/MYD88 signaling in neurodegenerative diseases
- The adaptive and maladaptive continuum of stress responses – a hippocampal perspective
- Role of leukemia inhibitory factor in the nervous system and its pathology
- Tracking markers of response inhibition in electroencephalographic data: why should we and how can we go beyond the N2 component?
- An explanation of the pathophysiology of adverse neurodevelopmental outcomes in iron deficiency
Articles in the same Issue
- Frontmatter
- Neuroprotective effects of geniposide on Alzheimer’s disease pathology
- Autophagy in Alzheimer’s disease
- Spinal cord injury: overview of experimental approaches used to restore locomotor activity
- Role of Toll-like receptor/MYD88 signaling in neurodegenerative diseases
- The adaptive and maladaptive continuum of stress responses – a hippocampal perspective
- Role of leukemia inhibitory factor in the nervous system and its pathology
- Tracking markers of response inhibition in electroencephalographic data: why should we and how can we go beyond the N2 component?
- An explanation of the pathophysiology of adverse neurodevelopmental outcomes in iron deficiency