Central nervous system aging and regeneration after injuries. A systematic approach.
Aging is associated with a decline of locomotor, sensory and cognitive performance in humans and experimental animals. Mechanistically, organismal senescence is caused by a gradual, lifelong accumulation of multifaceted molecular and cellular damage. Further, the rate and pattern of organismal senescence may be regulated in part by changes in multiple genes involved in multiple processes. While this theory is supported by genetic data in lower organisms, a lack of direct experimental evidence in higher organisms has contributed to a broader acceptance of the "stochastic aging" model, in which accumulating, random damaging biological events play an important role. However, these insults alone cannot account for the inexorable deterioration and loss of function that characterizes old biological systems of higher complexity like humans. Recent advances in unbiased gene expression profiling of the entire genome is a valuable tool for the study of complex biological phenomena such as aging. Using this technology, it is now possible to analyze in detail gene expression at the systems level. In the past decade with the advent of high-throughput technologies, biology has migrated from a descriptive science to a predictive. Most importantly, data from animal models has shown that senescent systems do retain some capacity for regeneration and functional recovery after injuries.
Department of Neurology, Clinic of Neurology, University of Greifswald, Germany. wagnerap@uni-greifswald.de
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Popa-Wagner
Stefania
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Crăiţoiu
Ana Maria
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Buga
D000375:Aging / Q000502:physiology*; D000818:Animals; D001921:Brain / Q000473:pathology / Q000502:physiology*; D001930:Brain Injuries / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D020925:Hypoxia-Ischemia, Brain / Q000473:pathology / Q000503:physiopathology; D023421:Models, Animal; D020411:Oligonucleotide Array Sequence Analysis; D051381:Rats; D012038:Regeneration; D020521:Stroke / Q000473:pathology / Q000503:physiopathology