Neuroinflamm-Aging and Neurodegenerative Diseases: An Overview
Vincenzo Pizza, Anella Agresta, Cosimo W. D'Acunto, Michela Festa and Anna Capasso
Affiliation: Department of Pharmaceutical Science, University of Salerno, Italy.
Keywords: Aging, neuroinflammation, neurodegenerative disease, Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, multiple sclerosis, psychiatric disorders, Alzheimers disease, Parkinsons Disease, Lymphocytic Remodelling, Free Radical Theory, Oxi-Inflamm-Aging Theory, Network theory, Cytomegalovirus, SOD1, Schezophrenia, Autism, Delirium, Epilepsy, Cerebral Ischemia
Neuroinflammation is considered a chronic activation of the immune response in the central nervous system (CNS) in response to different injuries. This brain immune activation results in various events: circulating immune cells infiltrate the CNS; resident cells are activated; and pro-inflammatory mediators produced and released induce neuroinflammatory brain disease. The effect of immune diffusible mediators on synaptic plasticity might result in CNS dysfunction during neuroinflammatory brain diseases. The CNS dysfunction may induce several human pathological conditions associated with both cognitive impairment and a variable degree of neuroinflammation. Furthermore, age has a powerful effect on enhanced susceptibility to neurodegenerative diseases and age-dependent enhanced neuroinflammatory processes may play an important role in toxin generation that causes death or dysfunction of neurons in neurodegenerative diseases This review will address current understanding of the relationship between ageing, neuroinflammation and neurodegenerative disease by focusing on the principal mechanisms by which the immune system influences the brain plastic phenomena. Also, the present review considers the principal human neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, multiple sclerosis and psychiatric disorders caused by aging and neuroinflammation.
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