Background And Objective: Cerebral small vessel disease (CSVD) often coexists with cognitive dysfunction in patients, leading to significant challenges in treatment and management. This study aimed to examine the efficacy of combined application of donepezil and nimodipine on patients with comorbid CSVD and cognitive dysfunction and the effects on patients' albumin and prealbumin levels.
Methods: The records of 112 patients with comorbid CSVD and cognitive dysfunction treated at the People's Hospital of Suzhou New District from January 2019 to December 2022 were analysed retrospectively.
Stroke can lead to cardiac complications such as arrhythmia, myocardial injury, and cardiac dysfunction, collectively termed stroke-heart syndrome (SHS). These cardiac alterations typically peak within 72 h of stroke onset and can have long-term effects on cardiac function. Post-stroke cardiac complications seriously affect prognosis and are the second most frequent cause of death in patients with stroke.
View Article and Find Full Text PDFRationale: Anti-ganglioside antibodies (AGA) play an essential role in the development of Miller-Fisher syndrome (MFS). The positive rate of ganglioside antibodies was exceptionally high in MFS, especially anti-GQ1b antibodies. However, the presence of other ganglioside antibodies does not exclude MFS.
View Article and Find Full Text PDFObjective: Thrombectomy greatly improves the clinical prognosis of patients with acute ischemic stroke (AIS). The aim of this study is to develop a nomogram model that can predict the prognosis of patients with acute ischemic stroke undergoing thrombectomy.
Methods: We retrospectively collected information of patients with acute ischemic stroke who were admitted to the stroke Green Channel of the First Affiliated Hospital of Soochow University from September 2018 to May 2022.
Objectives: The present study was designed to evaluate the effects of total cerebral small vessel disease (CSVD) on early-onset depression after acute ischemic stroke (AIS), and to develop a new nomogram including total CSVD burden to predict early-onset post-stroke depression (PSD).
Methods: We continuously enrolled patients with AIS who were hospitalized at the First Affiliated Hospital of Soochow University between October 2017 and June 2019. All patients were assessed for depressive symptoms using the 17-item Hamilton Depression Scale (HAMD-17) at 14 ± 2 days after the onset of AIS.
Neurogenesis plays an important role in the prognosis of stroke patients and is known to be promoted by the activation of the Notch1 signaling pathway. Studies on the airway epithelium have shown that miR-449b represses the Notch pathway. The study aimed to investigate whether limb remote ischemic conditioning (LRIC) was able to promote neurogenesis in cerebral ischemic mice, and to investigate the role of the miR-449b/Notch1 pathway in LRIC-induced neuroprotection.
View Article and Find Full Text PDFObjective: This study aimed to explore the effect of different administration routes of a low dose of tirofiban on acute ischemic stroke (AIS) patients with successful recanalization after endovascular treatment (EVT).
Methods: This is a cohort study that retrospectively analyzed data of patients with AIS who underwent EVT and achieved successful recanalization from a prospective registry. Eligible patients were divided into three groups according to their use of tirofiban.
Temporal lobe epilepsy (TLE) is a complex neurological disease, and its occurrence and development are closely related to the autophagy signaling pathway. However, the mechanism by which electroacupuncture (EA) affects the regulation of autophagy has not been fully elucidated. TLE gene chip dataset GSE27166 and data from rats without epilepsy (n = 6) and rats with epilepsy (n = 6) were downloaded from Gene Expression Omnibus.
View Article and Find Full Text PDFBackground: Atherosclerosis is the most common cause of ischemia stroke. Computed tomographic angiography (CTA) and digital subtraction angiography (DSA) are used to evaluate the degree of lumen stenosis. However, these examinations are invasive and can only reveal mild to moderate stenosis.
View Article and Find Full Text PDFApomorphine hydrochloride (APO) is known to be a dopamine receptor agonist, and has recently been found to be a novel drug for Alzheimer's disease (AD). We found that APO treatment ameliorated oxidative stress in an AD mouse model and specifically attenuated the hydrogen peroxide-induced p53-related apoptosis in the SH-SY5Y neuroblastoma cell line. To further understand the mechanism behind this action, we investigated the actions of APO on intracellular redox systems, such as the glutathione cycle and catalase.
View Article and Find Full Text PDFObjective: Intracellular amyloid β-protein (Aβ) contributes to neurodegeneration in Alzheimer disease (AD). Apomorphine (APO) is a dopamine receptor agonist for Parkinson disease and also protects against oxidative stress. Efficacy of APO for an AD mouse model and effects of APO on cell cultures are studied.
View Article and Find Full Text PDFPresenilin 1 (PS1) gene mutations are the major causes of early-onset familial Alzheimer's disease and are known to increase amyloid-beta42 (Abeta42) production as well as to promote apoptosis. We have recently reported that intracellular Abeta42 activates p53 mRNA expression and promotes p53-dependent apoptosis. Here, we examined the p53 mRNA and protein levels in cells transfected with wild-type and I143T/G384A mutant PS1 genes.
View Article and Find Full Text PDFPresenilin 1 (PS1) gene mutations are the major causes of early-onset familial Alzheimer's disease. Acceleration of apoptosis is one of the major pathogenic mechanisms of PS1 mutants, and PS1 mutants have also been reported to induce overproduction of amyloid-beta protein 42. Here, we investigated aberrancy in activation of initiator caspases related to two PS1 gene mutations, I143T and G384A.
View Article and Find Full Text PDFNihon Shinkei Seishin Yakurigaku Zasshi
April 2007
Inhibition of aggregation of amyloid p-protein (AP) and promotion of extracellular AM removal are known as potent therapeutic tools for Alzheimer's disease (AD). While, the importance of Af342 accumulating in neurons has recently been suggested, and we have reported that A/42 accumulating in the neurons moves into the nucleus, activating p53 mRNA expression and leading to apoptosis (Ohyagi et al, FASEB J, 2005). Moreover, intraneuronal Ap is reported to induce mitochondrial dysfunction via binding ABAD, synaptic pathology, and inhibition of proteasome.
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