Aging and disease
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Aging is characterized by increased oxidative stress, heightened inflammatory response, accelerated cellular senescence and progressive organ dysfunction. The homeostatic imbalance with aging significantly alters cellular responses to injury. Though it is unclear whether cellular energetic imbalance is a cause or effect of the aging process, preservation of mitochondrial function has been reported to be important in organ function restoration following severe injury. ⋯ Studies have identified alterations in the level or activity of factors such as SIRT1, PGC-1α, HIF-1α and c-MYC involved in key regulatory processes in the maintenance of mitochondrial structural integrity, biogenesis and function. Studies using experimental models of hemorrhagic injury and burn have demonstrated significant influence of aging in metabolic regulation and organ function. Understanding the age-associated molecular mechanisms regulating mitochondrial dysfunction following injury is important towards identifying novel targets and therapeutic strategies to improve the outcome after injury in the elderly.
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Sepsis is a serious problem among the geriatric population as its incidence and mortality rates dramatically increase with advanced age. Despite a large number of ongoing clinical and basic research studies, there is currently no effective therapeutic strategy that rescues elderly patients with severe sepsis. ⋯ The disparity between clinical and basic studies is a problem, and this is likely due, in part, to the fact that most laboratory animals used for sepsis research are not old while the majority of sepsis cases occur in the geriatric population. The objective of this article is to review recent epidemiological studies and clinical observations, and compare these with findings from basic laboratory studies which have used aged animals in experimental sepsis.
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Parkinson's disease is a chronic neurodegenerative disorder leading to progressive motor impairment affecting more than 1% of the over-65 population. In spite of considerable progress in identifying the genetic and biochemical basis of PD, to date the diagnosis remains clinical and disease-modifying therapies continue to be elusive. ⋯ Although none of these parameters has been validated for routine clinical practice yet, however some biochemical candidates hold great promise for application in PD patients, especially in the early stages of disease, and it is likely that in the future the diagnosis of PD will require a combination of genetic, imaging and laboratory data. In this review we discuss the most interesting biochemical markers for PD (including the "-omics" techniques), focusing on the methodological challenges in using ex vivo blood/CSF/tissue-based biomarkers and suggesting alternative strategies to overcome the difficulties that still prevent their actual use.
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Aging is an important and critical factor that contributes to the clinical outcome of burn patients. The very young and the elderly are more likely to succumb after major burn as compared to their adult counterparts. With the aging population, improved understanding of the mechanisms underlying age-associated complications after burns becomes even more demanding. ⋯ Age-associated immune dysfunction, immunosenescence, may predispose the elderly burn patients to more infections, slower healing and/or to other complications. Furthermore, pre-existing, age-related medical conditions such as, pulmonary/cardiovascular dysfunctions and diabetes in the elderly are other important factors that contribute to their poorer outcomes after major burn. The present review describes the impact of aging on burn patients outcomes.
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Older age has long been associated with altered inflammation and hemostasis regulation. Emerging evidence suggests that age-related differences in inflammation and hemostasis abnormalities may play a role in the development of and long-term outcomes after critical illness. A better understanding of underlying mechanisms may provide new possibilities for therapeutic interventions. In this review, we will examine how age-related differences in inflammatory and coagulation responses are affected through the continuum of healthy state, before infection occurs, to severe sepsis and recovery.