Neuroinflammation and ageing: current theories and an overview of the data.
The increase in the average lifespan and the consequent proportional growth of the elderly segment of society has furthered the interest in studying ageing processes. Ageing may be considered a multifactorial process derived from the interaction between genetic and environmental factors including lifestyle. There is ample evidence in many species that the maximum age attainable (maximum lifespan potential, MLSP) is genetically determined and several mitochondrial DNA polymorphisms are associated with longevity. This review will address the current understanding of the relationship between ageing and several factors both genetics and life style related. Firstly we focused on the most reliable and commonly shared theories which attempt to explain the phenomenon of ageing as the genetic, cellular, neuroendocrine, immunological and free-radicals related theories. Many studies have shown that most of the phenotypic characteristics observed in the aging process are the result of the occurrence, with age, of a low grade chronic pro-inflammatory status called "inflammaging", partially under genetic control. The term indicate that aging is accompanied by a low degree of chronic inflammatory, an up-regulation of inflammatory response and that inflammatory changes are common to many age-related diseases. In this review special attention was dedicated to diseases related to age as atherosclerosis, cancer and Alzheimer disease. Despite the fact that in recent years many theories about ageing have been developed, we are still far from a full understanding of the mechanisms underlying the ageing process.
Neurophysiopathology Unit, S. Luca Hospital, Vallo della Lucania (Sa), Italy.
Vincenzo
V
Pizza
Anella
A
Agresta
Cosimo W
CW
D'Acunto
Michela
M
Festa
Anna
A
Capasso
D000375:Aging / Q000235:genetics / Q000276:immunology* / Q000502:physiology*; D000544:Alzheimer Disease / Q000209:etiology; D017209:Apoptosis; D050197:Atherosclerosis / Q000209:etiology; D005075:Biological Evolution; D001921:Brain / Q000473:pathology; D016922:Cellular Senescence / Q000235:genetics; D016207:Cytokines / Q000378:metabolism; D003687:Dehydroepiandrosterone; D004777:Environment; D005609:Free Radicals / Q000378:metabolism; D013006:Growth Hormone; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology; D007113:Immunity, Innate; D007249:Inflammation / Q000150:complications / Q000503:physiopathology*; D008019:Life Style; D008550:Melatonin; D009369:Neoplasms / Q000209:etiology; D018384:Oxidative Stress / Q000502:physiology; D010913:Pituitary-Adrenal System / Q000502:physiology; D017382:Reactive Oxygen Species / Q000378:metabolism; D013601:T-Lymphocytes / Q000276:immunology; D016615:Telomere; D013950:Thymus Gland / Q000502:physiology
D016207:Cytokines; D005609:Free Radicals; D017382:Reactive Oxygen Species; D003687:Dehydroepiandrosterone; D013006:Growth Hormone; D008550:Melatonin