Neuroinflammation is a prevalent trait in virtually all neurological illnesses, making it one of the most researched areas in neuroscience. Although neuroinflammation's primary job is to defend the nervous system from an injury, the complicated and sequential response of activated glial cells can cause neurological damage. The inflammatory response can be neuroprotective, neurotoxic, or both depending on the kind of glial cell and the period after the injury. During neuroinflammation, numerous pathways are engaged, and several bioactive intermediates are produced. The kynurenine pathway, which catabolizes tryptophan and is involved in immunological control, neuroprotection, and neurotoxicity, is one of the most frequent. Various models have been utilised to investigate the kynurenine pathway metabolites' roles in the development and maintenance of inflammatory processes generated by infections. The parasite infection Neospora caninum, for example, might be utilised as a relevant model to investigate the involvement of the kynurenine pathway in the neuroinflammatory response and the fraction of cells participating. As the world's population ages, the prevalence of diagnosable neurological illnesses rises, indicating a negative impact on health and quality of life. Many investigations are being conducted to explore the possible roles of neuroinflammation in the aetiology of a variety of neurological illnesses. Although inflammatory processes may not cause such illnesses on their own, the immune system can have a significant impact on symptom severity and development. In such cases, scientists are currently exploring for therapeutic targets that might effectively reduce the increased immune responses associated with neuroinflammation.
