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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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TL;DR: The findings are consistent with a model of late-onset Alzheimer disease in which β-amyloidosis arises in later life on a background of preexisting structural and cognitive decline that is associated with aging and not with β-Amyloid deposits.
Abstract: Importance Typical cognitive aging may be defined as age-associated changes in cognitive performance in individuals who remain free of dementia. Ideally, the full adult age spectrum should be included to assess brain imaging findings associated with typical aging. Objective To compare age, sex, and APOE e4 effects on memory, brain structure (adjusted hippocampal volume [HVa]), and amyloid positron emission tomography (PET) in cognitively normal individuals aged 30 to 95 years old. Design, Setting, and Participants Cross-sectional observational study (March 2006 to October 2014) at an academic medical center. We studied 1246 cognitively normal individuals, including 1209 participants aged 50 to 95 years old enrolled in a population-based study of cognitive aging and 37 self-selected volunteers aged 30 to 49 years old. Main Outcomes and Measures Memory, HVa, and amyloid PET. Results Overall, memory worsened from age 30 years through the 90s. The HVa worsened gradually from age 30 years to the mid-60s and more steeply beyond that age. The median amyloid PET was low until age 70 years and increased thereafter. Memory was worse in men than in women overall ( P P APOE e4 status at any age. From age 70 years onward, APOE e4 carriers had significantly greater median amyloid PET than noncarriers. However, the ages at which 10% of the population were amyloid PET positive were 57 years for APOE e4 carriers and 64 years for noncarriers. Conclusions and Relevance Male sex is associated with worse memory and HVa among cognitively normal individuals, while APOE e4 is not. In contrast, APOE e4 is associated with greater amyloid PET (from age 70 years onward), while sex is not. Worsening memory and HVa occur at earlier ages than abnormal amyloid PET. Therefore, neuropathological processes other than β-amyloidosis must underlie declines in brain structure and memory function in middle age. Our findings are consistent with a model of late-onset Alzheimer disease in which β-amyloidosis arises in later life on a background of preexisting structural and cognitive decline that is associated with aging and not with β-amyloid deposits.

300 citations

Journal ArticleDOI
TL;DR: BDNF serum values are increased in early stages of Alzheimer’s disease, which may reflect a compensatory repair mechanism in early neurodegeneration and could also contribute to increased degradation of beta-amyloid (Abeta).
Abstract: Alzheimer’s disease (AD) is characterized by cognitive decline and loss of neurons in specific brain regions. Recent findings have suggested an involvement of brain-derived neurotrophic factor (BDNF) in the pathogenesis of AD. BDNF is an endogenous protein involved in the maintenance of neuronal function, synaptic plasticity and structural integrity in the adult brain.

300 citations

Journal ArticleDOI
TL;DR: The Subjective Cognitive Decline Initiative (SCD-I) Working Group is an international consortium established to develop a conceptual framework and research criteria for SCD (Jessen et al. as mentioned in this paper ).
Abstract: Research increasingly suggests that subjective cognitive decline (SCD) in older adults, in the absence of objective cognitive dysfunction or depression, may be a harbinger of non-normative cognitive decline and eventual progression to dementia. Little is known, however, about the key features of self-report measures currently used to assess SCD. The Subjective Cognitive Decline Initiative (SCD-I) Working Group is an international consortium established to develop a conceptual framework and research criteria for SCD (Jessen et al., 2014, Alzheimers Dement 10, 844-852). In the current study we systematically compared cognitive self-report items used by 19 SCD-I Working Group studies, representing 8 countries and 5 languages. We identified 34 self-report measures comprising 640 cognitive self-report items. There was little overlap among measures- approximately 75% of measures were used by only one study. Wide variation existed in response options and item content. Items pertaining to the memory domain predominated, accounting for about 60% of items surveyed, followed by executive function and attention, with 16% and 11% of the items, respectively. Items relating to memory for the names of people and the placement of common objects were represented on the greatest percentage of measures (56% each). Working group members reported that instrument selection decisions were often based on practical considerations beyond the study of SCD specifically, such as availability and brevity of measures. Results document the heterogeneity of approaches across studies to the emerging construct of SCD. We offer preliminary recommendations for instrument selection and future research directions including identifying items and measure formats associated with important clinical outcomes.

300 citations

Journal ArticleDOI
TL;DR: A direct association between cognitive activity and [(11)C]PiB uptake is reported, suggesting that lifestyle factors found in individuals with high cognitive engagement may prevent or slow deposition of β-amyloid, perhaps influencing the onset and progression of AD.
Abstract: The recent development of the radiopharmaceutical carbon 11–labeled Pittsburgh Compound B ([11C]PiB)1 has made it possible to image fibrillar forms of the β-amyloid (Aβ) protein, which is the major constituent of the amyloid plaque in Alzheimer disease (AD) Studies applying this technique have demonstrated [11C]PiB accumulation throughout cortex in most patients with AD More important, 20% to 30% of healthy, cognitively normal older individuals2,3 also display significant PiB uptake, which is consistent with evidence that some older individuals who were cognitively intact during life show substantial numbers of Aβ plaques post mortem4 Greater understanding of the factors associated with Aβ variability in the healthy older population could have important consequences for disease prevention Recent evidence indicates that lifestyle practices, such as increased physical exercise, are associated with reduced Aβ deposition based on [11C]PiB positron emission tomography (PET) and cerebrospinal fluid Aβ42 measurements5 Participation in cognitively stimulating activities has also been linked to reduced risk of late-life cognitive decline and AD6–8 An individual’s tendency to engage in physically and cognitively stimulating activities is likely related to a broad set of lifestyle factors that are difficult to quantify but include occupational, social, community, and recreational practices We assessed engagement in cognitive and physical activities and hypothesized that greater levels of engagement may be associated with less Aβ later in life We investigated this hypothesis by performing [11C]PiB PET and neuropsychological testing in a sample of cognitively normal older participants Aβ deposition, characterized as mean cortical [11C]PiB PET uptake, was examined in healthy older participants and comparison samples of young participants and patients with AD A variety of neuropsychological and lifestyle measurements were also obtained and assessed in relation to Aβ deposition for healthy older participants only, including frequency of engagement in cognitively demanding activities, frequency of engagement in physical and leisure activities, and current episodic memory function

299 citations

Journal ArticleDOI
TL;DR: Hippocampal volume was the primary determinant of memory decline, whereas executive function (EXEC) decline was related to multiple brain components, supporting a hypothesis that MEM decline is strongly influenced by Alzheimer disease (AD), whereas EXEC decline may be complexly determined by cerebrovascular disease and AD.
Abstract: Objective: To examine how baseline and change of volumetric MRI relate to cognitive decline in older individuals Background: Memory is associated with hippocampal integrity, whereas executive function has been linked to impaired frontal lobe function Previous studies have shown that hippocampal and cortical atrophy are more strongly related to cognition than are measures of subcortical cerebrovascular disease (CVD) The authors hypothesized that memory (MEM) decline would be related to change in hippocampal volume (HC), whereas decline in executive function (EXEC) would be related to change of cortical gray matter volume (CGM) and measures of subcortical CVD Methods: Subjects from a multicenter study (n = 103) included cognitively normal, mildly impaired, and demented cases with and without subcortical lacunes All had longitudinal cognitive evaluation (mean = 48 years) and two or more MRI scans at least one year apart (mean = 34 years) MRI measures included HC, CGM, total lacune volume (LAC), and white matter hyperintensity volume (WMH) Random effects modeling of longitudinal data assessed effects of MRI baseline and MRI change on baseline and change of psychometrically matched measures of MEM and EXEC Results: Change in MEM was related to HC baseline and HC change Change in EXEC was related to baseline CGM and to change in CGM, HC, and LAC Results were unchanged when demented cases were excluded WMH was not associated with change in MEM or EXEC independent of HC, CGM, and LAC Conclusion: Hippocampal volume was the primary determinant of memory decline, whereas executive function (EXEC) decline was related to multiple brain components Results support a hypothesis that MEM decline is strongly influenced by Alzheimer disease (AD), whereas EXEC decline may be complexly determined by cerebrovascular disease and AD

299 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