Dataset Information

Association of C-reactive protein with cognitive impairment.

ABSTRACT: High-sensitivity C-reactive protein (hsCRP) is a biomarker of cardiovascular risk that is suggested to be a biomarker for cognitive impairment.To explore the association between hsCRP and cognitive impairment.Cross-sectional analysis of a population-based community aging study.Northern Manhattan, New York, New York.One thousand three hundred thirty-one participants from a longitudinal study of aging without dementia and with available hsCRP and neuropsychological testing data at baseline.Four cognitive scores (memory, visuospatial, executive, and language impairment) derived from a neuropsychological battery. Cognitive impairment was defined by scores below 1.5 SDs of demographically corrected means.Participants in the highest hsCRP tertile had higher adjusted odds of impaired memory (odds ratio [OR], 1.5; 95% confidence interval [CI], 1.0-2.1; P = .03) than participants in the lowest tertile. Subjects in the highest hsCRP tertile also had greater odds of visuospatial impairment (OR, 1.6; 95% CI, 1.0-2.3; P = .03). Higher hsCRP was not associated with executive or language impairment. Persons with at least 1 APOE epsilon4 allele and hsCRP in the highest tertile had the greatest odds of impaired memory (OR, 2.7; 95% CI, 1.6-4.4).High hsCRP may be a marker of memory and visuospatial impairment in the elderly. The role of APOE epsilon4 requires further exploration.

SUBMITTER: Noble JM

PROVIDER: S-EPMC4426905 | biostudies-literature | 2010 Jan

REPOSITORIES: biostudies-literature

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Association of C-reactive protein with cognitive impairment.

Noble James M JM Manly Jennifer J JJ Schupf Nicole N Tang Ming Xing MX Mayeux Richard R Luchsinger José A JA

Archives of neurology 20100101 1

<h4>Background</h4>High-sensitivity C-reactive protein (hsCRP) is a biomarker of cardiovascular risk that is suggested to be a biomarker for cognitive impairment.<h4>Objective</h4>To explore the association between hsCRP and cognitive impairment.<h4>Design</h4>Cross-sectional analysis of a population-based community aging study.<h4>Setting</h4>Northern Manhattan, New York, New York.<h4>Other participants</h4>One thousand three hundred thirty-one participants from a longitudinal study of aging wi ...[more]

PMID: 20065134

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Project description:Background Previous studies revealed inconsistent results regarding association between migraine and cognitive impairment. In addition, previous studies found inconsistent results regarding the association between migraine and risk of dementia. Thus, the study aimed to make a meta-analysis exploring comparison result in different types of cognitive function between migraine patients and non-migraine subjects. In addition, meta-analysis was made to explore the association between migraine and risk of dementia. Methods Articles published before June 2022 were searched in the following databases: PubMed, Web of Science, SCOPUS, EMBASE, EBSCO, PROQUEST, ScienceDirect and Cochrane Database of Systematic Reviews. Results were computed using STATA 12.0 software. Results Meta-analysis showed lower general cognitive function and language function in migraine group, compared to no migraine group (general cognitive function: standard mean difference (SMD) = − 0.40, 95% CI = − 0.66 to − 0.15; language: SMD = − 0.14, 95% confidence interval (CI) = − 0.27 to − 0.00), whereas the study showed no significant difference in visuospatial function, attention, executive function and memory between migraine group and no migraine group (visuospatial function: SMD = − 0.23, 95% CI = − 0.53 to 0.08; attention: SMD = − 0.01, 95% CI = − 0.10 to 0.08; executive function: SMD = − 0.05, 95% CI = − 0.16 to 0.05; memory: SMD = − 0.14, 95% CI = − 0.30 to 0.03). In addition, the meta-analysis showed a significant association between migraine and risk of dementia (odds ratio (OR)/relative risk (RR) = 1.30, 95% CI = 1.11 to 1.52). Conclusions In conclusion, the meta-analysis demonstrated lower general cognitive function and language function in migraine. In addition, migraine is associated with an increased risk of all-cause dementia, VaD and AD. These results suggest a significant association between migraine and cognitive impairment. Because of the association between migraine and cognitive impairment, neurological physician should be vigilant and effectively intervene in migraineurs with high risk factors of cognitive impairment to prevent the development of cognitive impairment. Supplementary Information The online version contains supplementary material available at 10.1186/s10194-022-01462-4.

Project description:Although immediate early genes (IEGs) such as Bdnf, Arc and Egr1, have been implicated in plasticity, the larger pathways related to memory and memory disorders are not well understood. Here, we combined statistical Affymetrix microarray and behavioral analyses to identify key genes and pathways associated with aging-related cognitive impairment. Aged rats were separated into cognitively unimpaired (AU) or impaired (AI) groups, based on their Morris water maze performance relative to young-adult (Y) animals. Hippocampal gene expression was assessed in Y, AU and AI on the fifth (last) day of maze training or 21 days posttraining, and in non-trained aged and young animals (eight groups, overall n = 78, one chip/animal). ANOVA, linear contrasts, and overrepresentation analyses identified genes and pathways that differed from Y generally with aging (in both AU and AI) or selectively with cognitive status (only in AI or AU). Plasticity pathways, including insulin/cAMP/IEG signaling, and glycogenolytic and lipogenic pathways, were selectively downregulated (5 days) in AI, whereas Notch2 (regulating oligodendrocyte differentiation) and myelination pathways were upregulated (particularly at 21 days). Downregulation with general aging occurred in signal transduction and axonal growth/transport pathways, whereas upegulation occurred in immune/inflammatory, lipid metabolism/transport (e.g., Lxr-Srebf1), and lysosomal pathways. In AU, receptor/signal transduction genes were selectively upregulated, suggesting possible compensatory mechanisms. Immunohistochemistry confirmed and extended results to the protein level. Thus, this study identified novel cognition-linked processes, suggesting a new model in which energy-intensive, plasticity/lipogenic processes and energy-generating pathways necessary for learning are coordinately downregulated during training, while myelinogenic programs that impair cognition are concurrently activated. Keywords: Immediate Early Genes, Insulin Signaling, Cholesterol, Myelination, Glia, Inflammation, Young and Old comparaison, behavioral-characterization, Aging-related cognitive impairment.

Dataset Information

Association of C-reactive protein with cognitive impairment.

Publications

Association of C-reactive protein with cognitive impairment.

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