Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Background: Decreased cognitive function associated with coronary artery bypass graft surgery is common. These deficits may be similar to the cognitive dysfunction seen in the spectrum of mild cognitive impairment to Alzheimer's disease, which are believed to result from the accumulation of amyloid beta (Abeta) peptide in the brain. We measured cognition both before and after coronary artery bypass graft surgery and assayed Abeta levels to investigate whether the cognitive dysfunction of cardiac surgery was associated with Abeta levels.
Methods: The plasma of 332 patients, who had undergone neuropsychological testing before and 3 and 12 months after coronary artery bypass graft surgery, was analyzed for Abeta(42) and Abeta(40). Patients were classified as having preexisting cognitive impairment if cognitive function was decreased in two or more tests compared with a healthy control group, and postoperative cognitive dysfunction was defined as a decline in two or more tests compared with the group mean baseline score.
Results: Preexisting cognitive impairment was present in 117 patients (35.2%), and postoperative cognitive dysfunction was present in 40 (12%) at 3 months and 41 (13%) at 12 months after surgery. Both plasma Abeta(42) and Abeta(40) levels assessed before the surgery were significantly lower in patients who later had postoperative cognitive dysfunction at 3 months.
Conclusions: Decreased preoperative plasma levels of Abeta(42) and Abeta(40) in patients who exhibit postoperative cognitive dysfunction at 3 months suggest that postoperative cognitive dysfunction at this time may share a common mechanism with mild cognitive impairment and Alzheimer's disease. This process may be exacerbated by anesthesia.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.athoracsur.2009.07.003 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Cognitive Compensation Depends on Frontoparietal Network Structure-Function Coupling in Patients With White Matter Hyperintensity.
Brain Behav
September 2025
Department of Neurology, the Second Affiliated Hospital of Zhejiang University, School of Medicine, Hangzhou, China.
Background And Purpose: White matter hyperintensity (WMH) impairs cognitive function but is not evident in the early stage, raising the need to explore the underlying mechanism. We aimed to investigate the potential role of network structure-function coupling (SC-FC coupling) in cognitive performance of WMH patients.
Methods: A total of 617 participants with WMH (mean age = 61 [SD = 8]; 287 females [46.
TRPV1 Suppresses Microglial Inflammatory Activation to Ameliorate Schizophrenia-Associated Behaviors in Maternal Separation Rats.
Schizophr Bull
September 2025
Department of Psychiatry, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Background And Hypothesis: Schizophrenia is linked to hippocampal dysfunction and microglial inflammatory activation. Our prior clinical findings revealed significantly reduced transient receptor potential vanilloid 1 (TRPV1) expression in both first-episode and recurrent schizophrenia patients, with levels inversely correlating with symptom severity, implicating TRPV1 dysfunction in disease progression. Preclinical maternal separation (MS) models recapitulate schizophrenia-like behavioral and synaptic deficits, paralleled by hippocampal microglial TRPV1 downregulation.
View Article and Find Full Text PDFCognitive Abilities and Listening Effort in Individuals with Vestibular Migraine.
J Am Acad Audiol
September 2025
Given the evidence of cognitive deficits in individuals with vestibular dysfunction, reduced cognitive resources may impact the effort required to process auditory information, particularly in adverse listening conditions. Although existing literature suggests impaired performance on cognitive tasks in vestibular disorders in general, research in this area specific to patients with vestibular migraine is limited. This article aims to investigate working memory, auditory attention, and listening effort among individuals with vestibular migraine.
View Article and Find Full Text PDFComplement C4b as a Key Mediator of Synaptic Loss and Cognitive Decline in Brain Aging.
Mol Ther
September 2025
Department of Health Management & Institute of Health Management, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu 610054, China; Laboratory of Aging Research, School of Medicine, University of Electronic Science and Technology of China, Chengdu
Brain aging is a major risk factor for cognitive decline and neurodegenerative diseases, driven by synaptic loss, reduced synaptic function, and inflammation. However, the molecular mechanisms underlying these dysfunctions remain unclear. Here, we conducted comparative transcriptomic analyses of brain regions (cortex and hippocampus) and kidney tissues, a peripheral organ with documented age-related dysfunction.
View Article and Find Full Text PDFABCA7 variants impact phosphatidylcholine and mitochondria in neurons.
Nature
September 2025
Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA, USA.
Loss-of-function variants in the lipid transporter ABCA7 substantially increase the risk of Alzheimer's disease, yet how they impact cellular states to drive disease remains unclear. Here, using single-nucleus RNA-sequencing analysis of human brain samples, we identified widespread gene expression changes across multiple neural cell types associated with rare ABCA7 loss-of-function variants. Excitatory neurons, which expressed the highest levels of ABCA7, showed disrupted lipid metabolism, mitochondrial function, DNA repair and synaptic signalling pathways.
View Article and Find Full Text PDF