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Cognitive decline

About: Cognitive decline is a research topic. Over the lifetime, 29308 publications have been published within this topic receiving 1174689 citations.


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Journal ArticleDOI
TL;DR: It is likely that diffusion tensor imaging has the potential to emerge as a useful clinical tool for early detection and monitoring of disease progression and treatment response in mild cognitive impairment/Alzheimer's disease patients.
Abstract: Purpose of reviewTo provide a comprehensive review of diffusion tensor imaging in evaluating microstructural changes in the spectrum of cognitive decline from ageing to Alzheimer's disease, in particular focusing on mild cognitive impairment.Recent findingsMild cognitive impairment represents a tran

281 citations

Journal ArticleDOI
TL;DR: The findings suggest that interaction in larger social networks is a marker that portends less cognitive decline, and that distinct associational paths link interpersonal activity and emotional support to cognitive function.
Abstract: We examined the relationship between social network characteristics and global cognitive status in a community-based sample of 354 adults aged 50+ and with Mini-Mental State Examination (MMSE) scores of 28+ at baseline. Multivariate analyses indicated that interaction in larger social networks related to better maintenance of MMSE scores and reduced odds of decline to population-based lower quartile MMSE scores at follow-up 12 years later. At follow-up, higher levels of interpersonal activity (more frequent contacts in larger social networks) and exposure to emotional support independently related positively to MMSE. The findings suggest that interaction in larger social networks is a marker that portends less cognitive decline, and that distinct associational paths link interpersonal activity and emotional support to cognitive function.

280 citations

Journal ArticleDOI
TL;DR: Clinico-pathological studies and harmonization of neuropathological procedures are needed to validate the diagnostic criteria for VaD and mixed dementia in order to clarify the impact of CVLs and other coexistent pathologies on cognitive impairment as a basis for further successful therapeutic options.
Abstract: Vascular cognitive impairment describes a continuum of cognitive diorders ranging from mild cognitive impairment to dementia, in which vascular brain injury involving regions important for memory, cognition and behaviour plays an important role. Classification, prevalence, and pathophysiology are a matter of current research. Clinical diagnostic criteria show moderate sensitivity (ca 50%) and variable specificity (range 64-98%). In Western clinical series, VaD is suggested in 8-10% of cognitively impaired elderly subjects. Its prevalence in autopsy series varies from 0.03 to 58%. In contrast to Alzheimer disease (AD) and mixed dementia showing significant age-related increase, the prevalence of VaD significantly decreases after age 80 years. Cognitive decline is commonly associated with widespread small ischemic vascular lesions involving subcortical brain areas. The lesions affect neuronal networks involved in cognition, memory, and behavior. Cerebrovascular lesions (CVLs) often coexist wth Alzheimer-type lesions and other pathologies. The lesion pattern of "pure" VaD differs from that in mixed dementia (AD + CVLs), which suggests different pathogenesis of both phenotypes. Minor CVLs appear not essential for cognitive impairment in full-blown AD, while both mild AD-type pathology and small vessel disease may interact synergistically in promoting and progressing dementia. However, both AD-related and vascular brain pathologies have been reported. Despite recent suggestions for staging and grading CVLs in specific brain areas, no validated neuropathological criteria are currently available for VaD and mixed dementia. Further clinico-pathological studies and harmonization of neuropathological procedures are needed to validate the diagostic criteria for VaD and mixed dementia in order to clarify the impact of CVLs and other coexistent pathologies on cognitive impairment as a basis for further successful therapeutic options.

280 citations

Journal ArticleDOI
TL;DR: It is established that DG dysfunction is a driver of age-related cognitive decline and suggested non-pharmacological means for its amelioration are suggested.
Abstract: The dentate gyrus (DG) is a region in the hippocampal formation whose function declines in association with human aging and is therefore considered to be a possible source of age-related memory decline. Causal evidence is needed, however, to show that DG-associated memory decline in otherwise healthy elders can be improved by interventions that enhance DG function. We addressed this issue by first using a high-resolution variant of functional magnetic resonance imaging (fMRI) to map the precise site of age-related DG dysfunction and to develop a cognitive task whose function localized to this anatomical site. Then, in a controlled randomized trial, we applied these tools to study healthy 50-69-year-old subjects who consumed either a high or low cocoa flavanol-containing diet for 3 months. A high-flavanol intervention was found to enhance DG function, as measured by fMRI and by cognitive testing. Our findings establish that DG dysfunction is a driver of age-related cognitive decline and suggest non-pharmacological means for its amelioration.

280 citations

Journal ArticleDOI
TL;DR: A new model with accelerated tangle development is developed that completely prevents severe cognitive impairment in three different tests and indicates that immunotherapy targeting pathological tau is very feasible for tauopathies, and should be assessed in clinical trials in the near future.
Abstract: Harnessing the immune system to clear protein aggregates is emerging as a promising approach to treat various neurodegenerative diseases. In Alzheimer's disease (AD), several clinical trials are ongoing using active and passive immunotherapy targeting the amyloid-β (Aβ) peptide. Limited emphasis has been put into clearing tau/tangle pathology, another major hallmark of the disease. Recent findings from the first Aβ vaccination trial suggest that this approach has limited effect on tau pathology and that Aβ plaque clearance may not halt or slow the progression of dementia in individuals with mild-to-moderate AD. To assess within a reasonable timeframe whether targeting tau pathology with immunotherapy could prevent cognitive decline, we developed a new model with accelerated tangle development. It was generated by crossing available strains that express all six human tau isoforms and the M146L presenilin mutation. Here, we show that this unique approach completely prevents severe cognitive impairment in three different tests. This remarkable effect correlated well with extensive clearance of abnormal tau within the brain. Overall, our findings indicate that immunotherapy targeting pathological tau is very feasible for tauopathies, and should be assessed in clinical trials in the near future.

280 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
2023914
20221,895
20213,389
20202,982
20192,551
20182,022