Neurobiology of aging
-
Neurobiology of aging · Mar 2010
Age-related differences in pain sensitivity and regional brain activity evoked by noxious pressure.
Compared with young adults, older people report more chronic pain complaints, and show reduced tolerance to experimental pain. Atrophy of brain parenchyma in normal ageing is well documented, with grey matter reduction occurring across many regions known to be involved in pain processing. However, the functional consequences of these changes, in particular their contribution toward age-related differences in pain perception and report, are yet to be elucidated. ⋯ Both groups showed significant pain-related activity in a common network of areas including the insula, cingulate, posterior parietal and somatosensory cortices. However, compared with older adults, young subjects showed significantly greater activity in the contralateral putamen and caudate, which could not be accounted for by increased age-associated shrinkage in these regions. The age-related difference in pain-evoked activity seen in the present study may reflect reduced functioning of striatal pain modulatory mechanisms with advancing age.
-
Neurobiology of aging · Mar 2010
Quantitative fiber tracking of lateral and interhemispheric white matter systems in normal aging: relations to timed performance.
The integrity of white matter, as measured in vivo with diffusion tensor imaging (DTI), is disrupted in normal aging. A current consensus is that in adults advancing age affects anterior brain regions disproportionately more than posterior regions; however, the mainstay of studies supporting this anterior-posterior gradient is based primarily on measures of the corpus callosum. Using our quantitative fiber tracking approach, we assessed fiber tract integrity of samples of major white matter cortical, subcortical, interhemispheric, and cerebellar systems (11 bilateral and 2 callosal) on DTI data collected at 1.5T magnet strength. ⋯ By contrast, in women the age effect was present in both callosal regions, albeit modestly more so in the genu than splenium. Functional meaningfulness of these age-related differences was supported by significant correlations between DTI signs of white matter degradation and poorer performance on cognitive or motor tests. This survey of multiple fiber systems throughout the brain revealed a differential pattern of age's effect on regional FA and diffusivity and suggests mechanisms of functional degradation, attributed at least in part to compromised fiber microstructure affecting myelin and axonal morphology.
-
Neurobiology of aging · Jan 2010
Vascular risk factors and dementia in the general population aged >85 years: prospective population-based study.
The aim of this study was to evaluate the association between dementia and common vascular risk factors including blood pressure, blood lipids, homocysteine and diabetes mellitus in a population of very old people. This study is a 9-year follow-up prospective population-based study monitoring 339 non-demented subjects aged 85 years or over in the city of Vantaa, Southern Finland. ⋯ It seems that the contribution of vascular risk factors to the risk of dementia may be age-dependent and their role in the very old subjects may be mediated through their influence on cerebrovascular morbidity. Thus, prevention of stroke and diabetes mellitus may reduce the risk of cognitive decline in the very old.
-
Neurobiology of aging · Jan 2010
A novel anti-inflammatory role of NCAM-derived mimetic peptide, FGL.
Age-related cognitive deficits in hippocampus are correlated with neuroinflammatory changes, typified by increased pro-inflammatory cytokine production and microglial activation. We provide evidence that the neural cell adhesion molecule (NCAM)-derived mimetic peptide, FG loop (FGL), acts as a novel anti-inflammatory agent. Administration of FGL to aged rats attenuated the increased expression of markers of activated microglia, the increase in pro-inflammatory interleukin-1beta (IL-1beta) and the impairment in long-term potentiation (LTP). ⋯ We demonstrate that FGL enhanced interleukin-4 (IL-4) release from glial cells and IL-4 in turn enhanced neuronal CD200 in vitro. We provide evidence that the increase in CD200 is reliant on IL-4-induced extracellular signal-regulated kinase (ERK) signal transduction. These findings provide the first evidence of a role for FGL as an anti-inflammatory agent and identify a mechanism by which FGL controls microglial activation.
-
Neurobiology of aging · Mar 2009
Review Meta AnalysisBlood-brain barrier: ageing and microvascular disease--systematic review and meta-analysis.
Cerebral "microvascular" disease occurs in lacunar stroke, leukoaraiosis, vascular dementia and Alzheimer's disease. It may arise from or contribute to insidious damage to the blood-brain barrier (BBB). We systematically reviewed the literature for evidence that BBB permeability is altered in patients with manifestations of cerebral microvascular disease. ⋯ D. 0.60, 99% CI 0.30, 0.89, p<0.01). BBB permeability increases with normal ageing and may be an important mechanism in the initiation or worsening of cerebral microvascular disease. Further studies on the role of BBB permeability are urgently needed.