By Anja K. Leist, Jenni Kulmala, Fredrica Nyqvist

In fresh years, the purpose of analysis on getting older has shifted from prolonging existence to fostering fit and cognitively powerful outdated age. so one can enhance the standard of lifetime of older humans, we have to larger comprehend cognitive getting older in addition to physically aging.

Health and Cognition in previous Age assembles the cream of analysis throughout assorted scientific, psychological overall healthiness, and social disciplines, and demonstrates how this data can result in more desirable results for older humans. the 1st half this specialist quantity discusses biomedical and lifestyles path components in getting older, quite as they have an effect on cognition and future health in later existence. From there, potent ideas are the focal point: interventions and care courses to enhance psychological functioning and normal caliber of existence, and present coverage and perform principles in selling fit, lively, and cognitively strong getting older. jointly, those assorted chapters provide a multi-faceted method of realizing and editing what used to be previously the inevitable process growing older. A sampling of the coverage:

  • How the getting older procedure impacts the immune system.
  • Occupational gerontology – work-related determinants of outdated age healthiness and functioning.
  • Social, behavioral, and contextual impacts on cognitive functionality and decline.
  • Lifestyle elements within the prevention of dementia.
  • Understanding long term care results: traditional and behavioral economics.
  • Social capital, psychological health, and loneliness in older humans.

For gerontologists, sociologists, social staff, well-being psychologists, and others operating to enhance older people’s lives, Health and Cognition in outdated Age brings services, versatility, and self assurance to the desk.

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Extra resources for Health and Cognition in Old Age: From Biomedical and Life Course Factors to Policy and Practice

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It has been demonstrated that IGF-1 has neuroprotective properties, stimulates neurogenesis and synaptogenesis, regulates brain glucose metabolism, inhibits glial inflammation by antagonizing tumor necrosis factor α (TNFα), and promotes elimination of amyloid-beta (Aβ) from cerebral tissue. Exposure to ceramides results in altered glucose utilization with low ATP levels, Aβ accumulation and hyperphosphorylation of tau protein (Gasparini and Xu 2003; Tong and de la Monte 2009). Hyperglycemia can impair cognitive function by causing disruption of cerebral regional blood flow, neuronal osmotic changes and alterations in glucose transport through the hematoencephalic barrier (Brownlee 2005; Kodl and Seaquist 2008).

2004; Manschot et al. 2007). White matter hyperintensities are associated with high risk of stroke and dementia (Debette and Markus 2010). While the causal relationship between ischemic vascular events and cognitive decline is clear, less is known about cerebral microvascular disease and how it might contribute to the onset and progression of dementia (van Harten et al. 2006; Tiehuis et al. 2008). Several large studies have identified an independent association between retinal vascular changes (diabetic retinopathy) as a marker of cerebral microvascular disease, and executive function, psychomotor speed decline, slow gait and depressive mood (Lesage et al.

In advanced plaques, accumulation of ubiquitin conjugates and its correlation with apoptotic cell death suggests that proteasomal degradation is decreased. , genetically engineered mice lacking expression of uPAR, we have observed that the proteasomal activity in aortic tissue is lower than that in wild-type mice (Kiyan et al. 2012). Thus, impaired proteasomal degradation of myocardin may explain the delayed vascular remodeling after injury, which we have shown in uPAR-knockout mice using the carotid artery ligation model.

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