Association between BDNF rs6265 polymorphisms and postoperative cognitive dysfunction in Chinese Han Population

Xie, Songhui; Yu, Lei; Zhou, Mingming; Liu, Li; Lei, Daoyun; Han, Chao

doi:10.1002/brb3.1800

Cited by 7 publications

(9 citation statements)

References 41 publications

(37 reference statements)

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“…Such findings highlight the potential role of the BDNF Val66Met polymorphism in interfering with the abilities and performance of children with learning disorder. These outputs are in line with Dincheva et al (2012) and Xie et al (2020) who reported that the Val66Met polymorphism modulates aspects of cognitive functions even in healthy adults. Moreover, genetic association studies have stated that this polymorphism could be a possible risk factor for the development of neuropsychiatric disorders and their associated cognitive and memory impairments (Miranda et al 2019;Chen et al 2017).…”

Section: Discussionsupporting

confidence: 89%

BDNF Val66Met Polymorphism: Suggested Genetic Involvement in Some Children with Learning Disorder

et al. 2022

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Brain-derived neurotrophic factor (BDNF) plays an essential role in neuronal survival, especially in areas responsible for memory and learning. The BDNF Val66Met polymorphism has been described as a cognitive modifier in people with neuropsychiatric disorders. BDNF levels have been found to be low in children with learning disorder (LD). However, Val66Met polymorphism has not been studied before in such children. The aim was to investigate the presence of BDNF val66Met polymorphism in a group of children with specific LD and to verify its impact on their cognitive abilities. The participants in this cross-sectional study (N = 111) were divided into two groups: one for children with LD and the other for neurotypical (NT) ones. Children with LD (N = 72) were diagnosed according to the DSM-5 criteria. Their abilities were evaluated using Stanford–Binet Intelligence Scale, dyslexia assessment test, Illinois Test of Psycholinguistic Abilities, and phonological awareness test. Genotyping of BDNF Val66Met polymorphism was performed for all participants. The frequency of the Met allele was 26% among children with LD (6 children had homozygous, 26 had heterozygous genotype). The percentage of participants with deficits in reading, writing, and phonemic segmentation was higher in Met allele carriers when compared to non-Met allele carriers in LD group. The frequency of Met allele among NT children was 3.85% (0 homozygous, 3 children had heterozygous genotype) (p = 0.00001). The high frequency of Val66Met polymorphism among children with LD introduces the BDNF gene as a genetic modifier of learning performance in some children who manifest specific learning disorder (developmental dyslexia).

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Section: Discussionsupporting

confidence: 89%

BDNF Val66Met Polymorphism: Suggested Genetic Involvement in Some Children with Learning Disorder

et al. 2022

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“…44 This present study also confirmed the damage caused by ischemia-hypoxia to neurons (Figures 2 and 4). Many studies have confirmed that BDNF protects against ischemia-hypoxic injury, 45,46 partially by controlling the ion channels. 47 been widely accepted, 48,49 and re-establishing E/I homeostasis provided therapeutic potential against neurodevelopmental disorders.…”

Section: Discussionmentioning

confidence: 98%

Sub‐dose anesthetics combined with chloride regulators protect the brain against chronic ischemia–hypoxia injury

Yang

Wang

et al. 2023

CNS Neurosci Ther

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BackgroundCerebral ischemia–hypoxia leads to excitotoxicity‐mediated neuronal damage and cognitive dysfunction, especially in the elderly. Excessive intracellular [Cl−]i accumulation weakens γ‐aminobutyric acid (GABA) compensatory effects. Sub‐anesthetic dose of propofol protected the brain against ischemia–hypoxia, which was abolished by blocking Cl− efflux transporter K+/Cl− cotransporter 2 (KCC2). We aimed to determine whether low‐dose anesthetic combined with [Cl−]i regulators could restore the compensatory GABAergic system and improve cognitive function.MethodsChronic cerebral hypoxia (CCH) model was established by bilateral carotid artery ligation in aged rats. Sub‐dose of anesthetics (propofol and sevoflurane) with or without KCC2 agonist N‐ethylmaleimide (NEM) or Na+/K+/Cl− cotransporter 1 (NKCC1) antagonist bumetanide (BTN) was administered systemically 30 days post‐surgery. Primary rat hippocampal neuronal cultures were subjected to hypoxic injury with or without drug treatment. Memory function, hippocampal neuronal survival, GABAergic system functioning, and brain‐derived neurotrophic factor (BDNF) expressions were evaluated.ResultsSub‐anesthetic dose of combined propofol (1.2 μg mL−1) and sevoflurane [0.7 MAC (minimum alveolar concentration)] did not aggravate the hypoxic brain injury in rats or cell damage in neuronal cultures. Adding either BTN or NEM protected against hypoxic injury, associated with improved cognitive function in vivo, less intracellular accumulation of [Cl−]i, reduced cell death, restored GABAergic compensation, and increased BDNF expression both in vivo and in vitro.ConclusionSub‐anesthetic dose of propofol and sevoflurane is a recommended anesthesia regimen in at‐risk patients. Restoration of [Cl−]i homeostasis and GABAergic could further reduce the brain damage caused by ischemia–hypoxia.

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“…Положительная динамика, заключавшаяся в восстановлении уровня BDNF до референсных значений через 7 суток после оперативного вмешательства, может быть связана с тем, что повреждение нейронов, ассоциированное с воспалительными изменениями в структурах ЦНС, провоцирует превращение предшественника BDNF -proBDNF до зрелой и активной формы, что подтверждает высокий репаративный потенциал [7,8], однако первоначальный дефицит мозгового нейротрофического фактора, как уже нами было показано, путем построения ROC-кривой может быть предиктором и, вероятно, патогенетическим звеном в развитии ПКД (AUC 0,974, отличное качество модели). Причины данного предоперационного недостатка BDNF могут быть различны, нельзя исключать как роль генетического полиморфизма, приводящего к снижению базального уровня BDNF [10], так и возможность влияния иных опосредованных факторов, таких как повреждение мышц [4], нарушения в работе свертывающей-антисвертывающей системы крови и активации тромбоцитов [6].…”

Section: таблица 1 характеристика обследуемых пациентов и группы конт...unclassified

Role of S100b protein and BDNF in immunopathogenesis of neuroinflammation in the patients with induced immunocompromised state

Кныш

Маркелова

Zenina

et al. 2021

Russian Journal of Immunology

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Post-operation cognitive dysfunctions, related to mild manifestations of neurological pathology occuring after surgery, represent an important challenge for both fundamental and clinical medicine. The underlying phenomena of neuroinflammation are still poorly understood and discutable. The studies in immunopathogenesis of neuroinflammation may help in understanding the development of pathology and suggest ways to solve this problem. A special role for implementation of this process belongs to neuropeptides. Objective: to characterize immunopathogenesis of neuroinflammation in the individuals with immunocompromised state induced during aorto-coronary bypass surgery. A total of 110 patients with ischemic heart disease who underwent myocardial revascularization under extracorporeal circulation conditions were examined. Pathological neuroinflammation was recognized by development of postoperative cognitive dysfunction based on changing results of the cognitive examination (Montreal scale, MoCa test). The patients were tested before intervention, and on day 7 after surgery. According to the test results, all the patients were divided into 2 groups: (1) without signs of postoperative cognitive dysfunction and (2) with the mentioned signs. Venous blood was collected four times, on the day of surgery before the intervention, immediately after the surgery, 24 hours later, and on the 7th day after surgery. S100b and BDNF contents were determined in the venous blood serum. The baseline level of the S100b protein in the study groups did not differ from the reference values. After surgery, an increase in S100b was observed in both groups, but in patients with emerging postoperative cognitive dysfunction, these indexes were significantly higher. Despite a tendency for stabilization, the increased level of neuropeptides persisted 24 hours after the surgery; on the 7th day, the index was within the reference values, but in the 1st group it was lower than in the 2nd group. Prior to the operation, the BDNF level was significantly higher in the patients from group 1, compared with group 2. In the second group, the index was lower than the values obtained from the control group volunteers. After surgery, the values of BDNF in blood serum showed some differences: immediately after surgery, the level of neuropeptide was higher in patients without cognitive dysfunction. On day 7, the level of BDNF was within reference values, but in patients from group 2, the values were higher than in group 1.

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Association between BDNF rs6265 polymorphisms and postoperative cognitive dysfunction in Chinese Han Population

Cited by 7 publications

References 41 publications

BDNF Val66Met Polymorphism: Suggested Genetic Involvement in Some Children with Learning Disorder

BDNF Val66Met Polymorphism: Suggested Genetic Involvement in Some Children with Learning Disorder

Sub‐dose anesthetics combined with chloride regulators protect the brain against chronic ischemia–hypoxia injury

Role of S100b protein and BDNF in immunopathogenesis of neuroinflammation in the patients with induced immunocompromised state

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