Neural plasticity in the ageing brain

Burke, Sara N.; Barnes, Carol A.

doi:10.1038/nrn1809

Cited by 1,299 publications

(1,064 citation statements)

References 166 publications

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“…This is the first study to show clear evidence of hippocampal damage (volume losses and impairments in memory and learning) in type 2 diabetes, and may provide a window into very early manifestations of brain complications in type 2 diabetes. The hippocampus is more susceptible than other brain regions to damage by all sorts of insults, including severe hypoglycaemia and hypoxia [44,45]; thus, it is plausible that the hippocampus is the first region to be affected by type 2 diabetes, as our data appear to imply. We propose that, as the disease progresses and other risk factors associated with cardiovascular disease and the metabolic syndrome accumulate, more resilient brain areas are then also affected, as perhaps reflected by the occurrence of global atrophy and white matter pathology.…”

Section: Discussionmentioning

confidence: 47%

Hippocampal damage and memory impairments as possible early brain complications of type 2 diabetes

et al. 2007

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Aims/hypothesis There is evidence that type 2 diabetes mellitus is associated with cognitive impairment. Most studies investigating this association have evaluated elderly individuals, after many years of diabetes, who generally have poor glycaemic control and significant vascular disease. The aim of the current study was to investigate the early cognitive consequences and associated brain correlates of type 2 diabetes. Materials and methods With regard to cognition and brain measures, we compared 23 age-, sex-and educationmatched control subjects with 23 mostly middle-aged individuals with relatively well-controlled diabetes of less than 10 years from the time of diagnosis. Results We found deficits in hippocampal-based memory performance and preservation of other cognitive domains. Relative to control subjects, individuals with diabetes had reductions in brain volumes that were restricted to the hippocampus. There was an inverse relationship between glycaemic control and hippocampal volume; in multivariate regression analysis, HbA 1c was the only significant predictor of hippocampal volume, accounting for 33% of the observed variance. Other variables commonly associated with type 2 diabetes, such as elevated BMI, hypertension or dyslipidaemia, did not independently contribute to the variance in hippocampal volume. Conclusions/interpretation These results suggest that the medial temporal lobe may be the first brain site affected by type 2 diabetes and that individuals in poorer metabolic control may be affected to a greater extent.

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Section: Discussionmentioning

confidence: 47%

Hippocampal damage and memory impairments as possible early brain complications of type 2 diabetes

et al. 2007

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“…Research has shown that age-related changes in an array of neural and genetic responses may act as barriers to neuroplasticity and, potentially, recovery after brain injury and ischemia. 35,36 Recent evidence, however, has shown that middle-aged animals benefit from combination rehabilitation in a model of vascular dementia with resultant neuroplastic architectural changes accompanied by substantial improvements in cognition. 37 Further research is required to determine if similar increases in FosB/DFosB expression would be observed in aged animals using the current model of stroke.…”

Section: Discussionmentioning

confidence: 99%

Early Poststroke Experience Differentially Alters Periinfarct Layer II and III Cortex

Clarke

Langdon

Corbett

2014

J Cereb Blood Flow Metab

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Early poststroke rehabilitation effectively improves recovery of function, likely by engaging multiple plasticity processes through use-dependent activation of neural circuits. The loci of such neuroplastic reorganization have not been examined during the initial phase of behavioral recovery. In the current study, we sought to evaluate sub-components of rehabilitation and to identify brain sites first engaged by early rehabilitation. Rats were subjected to endothelin-1 ischemia and placed in either enriched environment (EE), daily reach training (RT), combination of enriched environment and reach training (ER), or standard housing (ST) starting 7 days post ischemia. Functional and histopathological assessments were made after 2, 5, and 10 days of treatment. Animals exposed to 10 days of ER treatment exhibited significantly more use-dependent neuronal activity (FosB/DFosB expression) in perilesional cortex than those exposed to EE, RT, or ST treatments. Similar trends were observed in both perilesional striatum and contralesional forelimb motor cortex. This use-dependent plasticity was not explained by differences in neuronal death, inflammation, or lesion volume. The increased activity likely contributes to the neuroplastic changes and functional recovery observed after extended periods of rehabilitation. Importantly, EE or RT alone did not lead to enhanced activity suggesting that combination therapy is necessary to promote maximum recovery.

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“…A more recent study in human also showed that very old individuals have comparable number of neocortical neurons to younger individuals, while there is significant difference in the total number of neocortical oligodendrocytes (Fabricius, Jacobsen, & Pakkenberg, 2013). Overall, cell counting methods show that significant neuron loss does not occur during normal aging and changes are subtle and region‐specific (Burke & Barnes, 2006). A special case in successful aging is cognitive intact elderly with AD pathology, which are believed to have resistant mechanism for Aβ oligomers, and Aβ oligomers are absent from hippocampal postsynapses, while Zn 2+ levels are lower in such cases (Bjorklund et al, 2012).…”

Section: Cellular Changes In Aging and Admentioning

confidence: 99%

Aging and Alzheimer’s disease: Comparison and associations from molecular to system level

et al. 2018

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Alzheimer's disease is the most prevalent cause of dementia, which is defined by the combined presence of amyloid and tau, but researchers are gradually moving away from the simple assumption of linear causality proposed by the original amyloid hypothesis. Aging is the main risk factor for Alzheimer's disease that cannot be explained by amyloid hypothesis. To evaluate how aging and Alzheimer's disease are intrinsically interwoven with each other, we review and summarize evidence from molecular, cellular, and system level. In particular, we focus on study designs, treatments, or interventions in Alzheimer's disease that could also be insightful in aging and vice versa.

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Neural plasticity in the ageing brain

Cited by 1,299 publications

References 166 publications

Hippocampal damage and memory impairments as possible early brain complications of type 2 diabetes

Hippocampal damage and memory impairments as possible early brain complications of type 2 diabetes

Early Poststroke Experience Differentially Alters Periinfarct Layer II and III Cortex

Aging and Alzheimer’s disease: Comparison and associations from molecular to system level

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