Inflammatory reactions in the central nervous system (CNS) are currently known to be associated with many neurological disorders. In neurodegenerative diseases, such as Alzheimer’s disease (AD) and Parkinson’s disease (PD), there is considerable penetration of different leukocyte subsets into the CNS or there is severe activation of microglial cells which increases many inflammatory mediators in the CNS. In acute CNS disorders, including delayed corrosion associated with vasospasm after subarachnoid hemorrhage (SAH), ischemic stroke, spontaneous intracerebral hemorrhage (ICH), and traumatic brain injury (TBI), current evidence from a variety of research studies reveal that inflammation may be a possible target for treatment. Inflammation is becoming a promising region of research study for new treatments.
To speed up the process of translating this information to clinical applications, a number of significant problems have to be addressed as their capacity to continuously identify characteristic cerebral deficits in people with neurodegenerative diseases, the connections of brain injuries to clinical symptoms and genetic diagnosis as well as the level to which the harm respond to various treatment approaches. In this article, findings that address some of these problems are reported by several researchers.
Neuroinflammation is ultimately characterized as the inflammation of the nervous tissue. It can commonly occur due to a variety of factors, including toxins, infections, autoimmune diseases, and even traumatic brain injury (TBI). In the central nervous system (CNS), the microglial cells are in charge of activating inflammatory reactions associated with these factors. However, excess microglia activation can ultimately cause a variety of health issues, including neurological diseases, among others. For more information, please feel free to ask Dr. Alex Jimenez or contact us at (915) 850-0900.