The role of inflammatory mediators in the central nervous system has been investigated in different types of neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease. Interestingly, these inflammatory mediators have a dual role in both proinflammatory and anti-inflammatory processes, upregulating and suppressing cellular damage in injury sites, respectively. Immediately upon injury or stress, the first and foremost responses are initiated by immune cells in the brain called microglia. The current literature has demonstrated that innate immunity is mostly involved in the mediation of molecular pathology in neurodegenerative diseases through Toll-like receptors (TLRs) which are present in microglia. To date, more than ten TLR subtypes have been identified in animals and humans. They are functionally dissimilar and have diverse roles in the modulation of innate immunity under pathological conditions. Hence, elucidating the crucial mechanisms mediating cellular damage through TLRs may lead to new insights for establishing therapeutic approaches to prevent neuronal and astrocytic damage in neurodegenerative diseases.

This special issue aims to collect original research and review articles dealing with TLR involvement in pathological conditions in neurodegenerative diseases. Researchers and clinicians are invited to submit articles relating to basic, translational, or clinical research investigating TLR involvement in cellular damage in neurodegenerative diseases. The submission of new methodologies to visualize cellular damage using new staining and analysis methods is also welcomed.

Potential topics include but are not limited to the following:

• TLR-mediated cellular damage in neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease
• Neuronal and astrocytic damage mediated through TLRs as a consequence of brain tumor or traumatic brain injury
• The effects of epilepsy, stress, and alcohol-addiction on neuroinflammation through TLRs, leading to cellular damage
• TLR-mediated pathological conditions in ischemia and hypoxia