Background: Cardiopulmonary bypass (CPB) elicits a systemic inflammatory response that may impair blood-brain barrier (BBB) integrity. BBB disruption can currently be detected by dynamic contrast enhancement magnetic resonance imaging (MRI), reflected by an increase in the permeability constant (K). We aimed to determine (1) whether CPB induces BBB disruption, (2) duration until BBB disruption resolution, and (3) the obtainable correlation between BBB injury (location and intensity) and neurocognitive dysfunction.
Methods: Seven patients undergoing CPB with coronary artery bypass grafting (CABG) were assigned to serial cerebral designated MRI evaluations, preoperatively and on postoperative day (POD) 1 and 5. Examinations were analyzed for BBB disruption and microemboli using dynamic contrast enhancement MRI and diffusion-weighted imaging methods, respectively. Neuropsychologic tests were performed 1 day preoperatively and on POD 5.
Results: A significant local K increase (0.03 min vs 0.07 min, p = 0.033) compatible with BBB disruption was evident in 5 patients (71%) on POD 1. Resolution was observed by POD 5 (mean, 0.012 min). The location of the disruption was most prominent in the frontal lobes (400% vs 150% K levels upsurge, p = 0.05). MRI evidence of microembolization was demonstrated in only 1 patient (14%). The postoperative global cognitive score was reduced in all patients (98.2 ± 12 vs 95.1 ± 11, p = 0.032), predominantly in executive and attention (frontal lobe-related) functions (91.8 ± 13 vs 86.9 ± 12, p = 0.042). The intensity of the dynamic contrast enhancement MRI BBB impairment correlated with the magnitude of cognition reduction (r = 0.69, p = 0.04).
Conclusions: BBB disruption was evident in most patients, primarily in the frontal lobes. The location and intensity of the BBB disruption, rather than the microembolic load, correlated with postoperative neurocognitive dysfunction.
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http://dx.doi.org/10.1016/j.athoracsur.2016.10.043 | DOI Listing |
Alzheimers Dement
December 2024
VIB-UGent Center for Inflammation Research, Ghent, Belgium.
Background: The brain is shielded from the peripheral circulation by central nervous system (CNS) barriers, comprising the well-known blood-brain barrier (BBB) and the less recognized blood-cerebrospinal fluid (CSF) barrier located within the brain ventricles. The gut microbiota represents a diverse and dynamic population of microorganisms that can influence the health of the host, including the development of neurological disorders like Alzheimer's disease (AD). However, the intricate mechanisms governing the interplay between the gut and brain remain elusive, and the means by which gut-derived signals traverse the CNS barriers remain unclear.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
The UC Irvine Institute for Memory Impairments and Neurological Disorders (UCI MIND), Irvine, CA, USA.
Background: Individuals with Down syndrome (DS) have an increased genetic risk of developing Alzheimer's disease (AD), with most adults developing AD neuropathology in their 40s. Despite having a low frequency of systemic vascular risk factors such as hypertension and atherosclerosis, adults with DS display cerebrovascular pathology, including microbleeds, microinfarcts, and cerebral amyloid angiopathy. This suggests that blood-brain barrier (BBB) integrity may be compromised allowing the extravasation of blood proteins in the brain parenchyma.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Johns Hopkins University, Saint Petersburg, FL, USA.
Background: Argonaute2 (Ago2) plays an essential role in RISC-mediated silencing of target mRNAs, which are critical for cellular functions. Argonaute2 Syndrome, also known as Ago2 Syndrome, is a rare neurological disorder recently discovered in humans. It has significant implications for brain development, yet it remains unstudied to date METHOD: To study this effect, we deleted the Ago2 gene in GABAergic (Slc32a1 cre) and Glutamatergic (Slc17a6 cre) mice.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Kentucky, Lexington, KY, USA.
Background: The APOE ε4 allele is the most prominent genetic predisposition for sporadic Alzheimer's disease (AD). Amylin, a neuroendocrine hormone co-secreted with insulin from the pancreas, is increased in blood in AD and readily forms neurotoxic homo- and hetero-oligomers with β-amyloid in AD. Previously, we showed that intravenously infused ApoE4 in rats expressing human amylin specifically in the pancreas led to increased brain amylin accumulation.
View Article and Find Full Text PDFShock
December 2024
Department of Pathology and Pathophysiology, Faculty of Basic Medical Science, Kunming Medical University, Kunming 650500, Yunnan, China.
Background: Sepsis-associated encephalopathy (SAE) represents a severe complication of sepsis, substantially elevating both mortality and healthcare costs for patients. Gastrodin (GAS), a principal bioactive constituent of Gastrodia elata Blume, is neuroprotective in various neurological disorders, including ischemic stroke, epilepsy, Alzheimer's disease, and neuropathic pain. In this study, we sought to investigate whether GAS could serve as a protective agent against SAE.
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