Dataset Information

Neural correlates of domain-specific cognitive decline: The ARIC-NCS Study.

ABSTRACT:

Objective

To evaluate the association of cognitive declines in the domains of memory, language, and executive function with brain gray matter (GM) volume in old age.

Methods

This was a prospective study of 1,846 participants in the Atherosclerosis Risk in Communities (ARIC) Study who underwent 3T brain MRI scans in 2011 to 2013. Participants were categorized by cognitive domain performance trajectory over the prior 20 years (cut point to define decline: 20th percentile). Associations between GM volume and cognitive declines were assessed at the voxel level with voxel-based morphometry and at the regional level with atlas-defined GM volumes of specific regions of interest.

Results

Participants were an average age of 76 years; 60% were female; and 28% were black. Participants in the top 20th percentile for decline in the memory domain had smaller GM volumes in the medial temporal lobe (-3.3%, 95% confidence interval [CI] -4.6% to -2.1%), amygdala (-2.7%, 95% CI -4.1% to -1.3%), entorhinal cortex (-4.1%, 95% CI -6.0% to -2.2%), and hippocampus (-3.8%, 95% CI -5.2% to -2.4%) compared to participants who were in the lowest 80th percentile for decline in all domains. In contrast, among participants who were in the top 20th percentile for decline in the language or executive function domains, GM volumes were smaller in more brain regions.

Conclusions

Declines in memory function were associated with brain volume loss in the medial temporal and hippocampal formations. Declines in language and executive function were associated with decreases in brain volumes across more noncontiguous brain regions.

SUBMITTER: Schneider ALC

PROVIDER: S-EPMC6442014 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:Background Abnormal P-wave indices (PWIs)-reflecting underlying left atrial abnormality-are associated with increased risk of stroke independent of atrial fibrillation. We assessed whether abnormal PWIs are associated with incident dementia and greater cognitive decline, independent of atrial fibrillation and ischemic stroke. Methods and Results We included 13 714 participants (mean age, 57±6 years; 56% women; 23% black) who were followed for dementia through the end of 2015. (Abnormal P-wave terminal force in lead V1, ≥4000 μV×ms), abnormal P-wave axis (>75° or <0°), prolonged P-wave duration (>120 ms), and advanced interatrial block were determined from ECGs at visits 2 to 4. Dementia was adjudicated by an expert panel using data from cognitive tests and hospitalization International Classification of Diseases codes. Cognitive function was measured longitudinally using 3 neuropsychological tests. Cox proportional hazards models were used to assess the association between time-dependent abnormal PWIs with incident dementia. Linear regression models were used to evaluate PWIs with cognitive function over time. At the conclusion of the study, 19%, 16%, 28%, and 1.9% of participants had abnormal P-wave terminal force in lead V1, abnormal P-wave axis, prolonged P-wave duration, and advanced interatrial block, respectively. During mean follow-up of 18 years, there were 1390 (10%) dementia cases. All abnormal PWIs except advanced interatrial block were associated with an increased risk of dementia even after adjustment for incident atrial fibrillation and stroke: multivariable hazard ratio of abnormal P wave terminal force in lead V1=1.60, 95% CI, 1.41 to 2.83; abnormal P-wave axis, hazard ratio =1.36, 95% CI, 1.17 to 2.57; prolonged P-wave duration, hazard ratio=1.60, 95% CI, 1.42 to 1.80. Only abnormal P-wave terminal force in lead V1 was associated with greater decline in global cognition. Conclusions Abnormal PWIs are independently associated with an increased risk of dementia. This novel finding should be replicated in other cohorts and the underlying mechanisms should be evaluated.

Project description:BackgroundVascular risk factors, including inflammation, may contribute to dementia development. We investigated the associations between peripheral inflammatory biomarkers and cognitive decline in five domains (memory, construction, language, psychomotor speed, and executive function).MethodsCommunity-dwelling older adults from the Ginkgo Evaluation of Memory Study (n = 1,159, aged 75 or older) free of dementia at baseline were included and followed for up to 7 years. Ten biomarkers were measured at baseline representing different sources of inflammation: vascular inflammation (pentraxin 3 and serum amyloid P), endothelial function (endothelin-1), metabolic function (adiponectin, resistin, and plasminogen activating inhibitor-1), oxidative stress (receptor for advanced glycation end products), and general inflammation (interleukin-6, interleukin-2, and interleukin-10). A combined z-score was created from these biomarkers to represent total inflammation across these sources. We utilized generalized estimating equations that included an interaction term between z-scores and time to assess effect of inflammation on cognitive decline, adjusting for demographics (such as age, race/ethnicity, and sex), cardiovascular risk factors, and apolipoprotein E ε4 carrier status. A Bonferroni-adjusted significance level of .01 was used. We explored associations between individual biomarkers and cognitive decline without adjustment for multiplicity.ResultsThe combined inflammation z-score was significantly associated with memory and psychomotor speed (p < .01). Pentraxin 3, serum amyloid P, endothelin-1, and interleukin-2 were associated with change in at least one cognitive domain (p < .05).ConclusionOur results suggest that total inflammation is associated with memory and psychomotor speed. In particular, systemic inflammation, vascular inflammation, and altered endothelial function may play roles in domain-specific cognitive decline of nondemented individuals.