Drugs to Treat Neuroinflammation in Neurodegenerative Disorders


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Аннотация

Neuroinflammation is associated with disorders of the nervous system, and it is induced in response to many factors, including pathogen infection, brain injury, toxic substances, and autoimmune diseases. Astrocytes and microglia have critical roles in neuroinflammation. Microglia are innate immune cells in the central nervous system (CNS), which are activated in reaction to neuroinflammation-inducing factors. Astrocytes can have pro- or anti-inflammatory responses, which depend on the type of stimuli presented by the inflamed milieu. Microglia respond and propagate peripheral inflammatory signals within the CNS that cause low-grade inflammation in the brain. The resulting alteration in neuronal activities leads to physiological and behavioral impairment. Consequently, activation, synthesis, and discharge of various pro-inflammatory cytokines and growth factors occur. These events lead to many neurodegenerative conditions, such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis discussed in this study. After understanding neuroinflammation mechanisms and the involvement of neurotransmitters, this study covers various drugs used to treat and manage these neurodegenerative illnesses. The study can be helpful in discovering new drug molecules for treating neurodegenerative disorders.

Об авторах

Yao-Chin Wang

Graduate Institute of Injury Prevention and Control, College of Public Health,, Taipei Medical University

Email: info@benthamscience.net

Woon-Man Kung

Department of Exercise and Health Promotion, College of Kinesiology and Health,, Chinese Culture University

Email: info@benthamscience.net

Yi-Hsiu Chung

Department of Medical Research and Development,, Linkou Chang Gung Memorial Hospital,

Автор, ответственный за переписку.
Email: info@benthamscience.net

Sunil Kumar

Graduate Institute of Natural Products, College of Medicine, Chang Gung University

Автор, ответственный за переписку.
Email: info@benthamscience.net

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