Association of HbA1c with functional outcome by ischemic stroke subtypes and age.

Objectives: To determine whether high HbA1c levels are related to short-and long-term functional outcomes in patients with ischemic stroke (IS) and whether this association differs according to the IS subtype and the patient's age.

Methods: The data of 7,380 IS patients admitted to 16 hospitals or regional stroke centers in South-Korea, between May 2017 and December 2019, were obtained from the Clinical Research Collaboration for Stroke-Korea-National Institute of Health database and retrospectively analyzed. Among these patients, 4,598 were followed-up for one-year.

Gender differences in mortality and long-term functional outcomes after first-ever ischemic stroke: A prospective cohort study.

Background: Although many studies about survival rates and functional outcomes after stroke have been published, studies on gender differences have reported conflicting results.

Aims: To determine whether there are differences in mortality and functional outcomes during the first 5 years after a first-ever ischemic stroke in Korean males and females.

Method: This is an interim analysis of the Korean Stroke Cohort for Functioning and Rehabilitation, a prospective multicenter cohort study.

Association between blood lead level and risk of stroke in Korean adults: a cross-sectional study in the Korea National Health and Nutrition Examination Survey 2008-2013.

Objectives: Although lead is a potential risk factor for cardiovascular diseases such as stroke, research on this association in the Korean population remains limited. Therefore, we aimed to investigate the association between lead level and stroke in Korean adults.

Design: A population-based cross-sectional study.

Association of Blood Cadmium with Cardiovascular Disease in Korea: From the Korea National Health and Nutrition Examination Survey 2008-2013 and 2016.

Cardiovascular disease (CVD) is the leading cause of death globally, although the mortality rate has declined with improved technology and risk factor control. The incidence rate of stroke, one of the CVDs, is increasing in young adults, whereas it is decreasing in the elderly. The risk factors for CVD may differ between young adults and the elderly.

Factors Associated with Changes in Functional Independence after Six Months of Ischemic Stroke.

The aim of this study is to investigate the changes in functional independence and their associated factors during the first 6 months to 1 year after stroke onset. This study is the interim results of the Korean Stroke Cohort for Functioning and Rehabilitation. A total of 1,011 participants were included and classified into 3 subgroups according to changes in the Korean version of Modified Barthel Index (K-MBI) scores that occurred between 6 months to 1 year after stroke onset: the improved group (IG), with scores that increased 5 points or more; the stationary group (SG), with the K-MBI score changes ranging from -4 to +4 points; and the declined group (DG), with the K-MBI scores that decreased 5 points or more.

Elevated Cerebrospinal Fluid and Plasma N-Cadherin in Alzheimer Disease.

N-cadherin is a synaptic adhesion molecule stabilizing synaptic cell structure and function. Cleavage of N-cadherin by γ-secretase produces a C-terminal fragment, which is increased in the brains of Alzheimer disease (AD) patients. Here, we investigated the relationship between fluid N-cadherin levels and AD pathology.

Elevation of plasma soluble amyloid precursor protein beta in Alzheimer's disease.

Introduction: Beta-amyloid is considered to be a pathophysiological marker in Alzheimer's disease (AD). Soluble amyloid precursor proteins (sAPPs) -α (sAPPα) and -β (sAPPβ), which are the byproducts of non-amyloidogenic and amyloidogenic process of APP, respectively, have been repeatedly observed in the cerebrospinal fluids (CSF) of AD patients. The present study focused on the determination of sAPP levels in peripheral blood.

Altered expression of Notch1 in Alzheimer's disease.

Notch signaling is an evolutionarily conserved pathway that regulates cell-cell interactions through binding of Notch family receptors to their cognate ligands. Notch signaling has an essential role in vascular development and angiogenesis. Recent studies have reported that Notch may be implicated in Alzheimer's disease (AD) pathophysiology.

Association of plasma endothelial lipase levels on cognitive impairment.

Background: Peripheral high-density lipoprotein cholesterol (HDL-C) has been known to influx into the brain and be inversely associated with the risk of Alzheimer's disease (AD). However, recent prospective studies of the association between HDL-C and AD have yielded inconsistent results. Here, we examined the association between the endothelial lipase (EL), which is known to be major determinant of HDL-C levels, and cognitive function.

Different Brain Connectivity between Responders and Nonresponders to Dual-Mode Noninvasive Brain Stimulation over Bilateral Primary Motor Cortices in Stroke Patients.

Noninvasive brain stimulation (NBS), such as repetitive transcranial magnetic stimulation (rTMS) or transcranial direct current stimulation (tDCS), has been used in stroke patients with motor impairment. NBS can help recovery from brain damage by modulating cortical excitability. However, the efficacy of NBS varies among individuals.

Fisetin stimulates autophagic degradation of phosphorylated tau via the activation of TFEB and Nrf2 transcription factors.

The neuronal accumulation of phosphorylated tau plays a critical role in the pathogenesis of Alzheimer's disease (AD). Here, we examined the effect of fisetin, a flavonol, on tau levels. Treatment of cortical cells or primary neurons with fisetin resulted in significant decreases in the levels of phosphorylated tau.

Plasma SUMO1 Protein is Elevated in Alzheimer's Disease.

Alzheimer's disease (AD) is the most common type of dementia in the elderly. The accumulation of amyloid-β peptides and tau proteins is the major pathogenic event of AD. There is accumulating evidence that both tau and amyloid-β linked to the small ubiquitin-like modifier (SUMO), which is increased in the brain of AD model mouse.

Aging-related Changes in Mouse Serum Glycerophospholipid Profiles.

Objectives: Metabolic dysfunction is a common hallmark of the aging process and aging-related pathogenesis. Blood metabolites have been used as biomarkers for many diseases, including cancers, complex chronic diseases, and neurodegenerative diseases.

Methods: In order to identify aging-related biomarkers from blood metabolites, we investigated the specific metabolite profiles of mouse sera from 4-month-old and 21-month-old mice by using a combined flow injection analysis-tandem mass spectrometry and liquid chromatography-tandem mass spectrometry.

SUMO1 promotes Aβ production via the modulation of autophagy.

Autophagy is one of the main mechanisms in the pathophysiology of neurodegenerative disease. The accumulation of autophagic vacuoles (AVs) in affected neurons is responsible for amyloid-β (Aβ) production. Previously, we reported that SUMO1 (small ubiquitin-like modifier 1) increases Aβ levels.

NDP52 associates with phosphorylated tau in brains of an Alzheimer disease mouse model.

We previously showed that NDP52 (also known as calcoco2) plays a role as an autophagic receptor for phosphorylated tau facilitating its clearance via autophagy. Here, we examined the expression and association of NDP52 with autophagy-regulated gene (ATG) proteins including LC3, as well as phosphorylated tau and amyloid-beta (Aβ) in brains of an AD mouse model. NDP52 was expressed not only in neurons, but also in microglia and astrocytes.

Sulforaphane induces autophagy through ERK activation in neuronal cells.

Sulforaphane (SFN), an activator of nuclear factor E2-related factor 2 (Nrf2), has been reported to induce autophagy in several cells. However, little is known about its signaling mechanism of autophagic induction. Here, we provide evidence that SFN induces autophagy with increased levels of LC3-II through extracellular signal-regulated kinase (ERK) activation in neuronal cells.

γ-Secretase-dependent cleavage of E-cadherin by staurosporine in breast cancer cells.

E-cadherin is a transmembrane protein that serves as a cell adhesion molecule component of the adherens junction. We previously showed that cadmium induced γ-secretase-dependent E-cadherin cleavage via oxidative stress. In this study, we report that staurosporine (STS)-induced apoptosis induces caspase-2 and/or -8-dependent E-cadherin cleavage.

Plasma carbonic anhydrase II protein is elevated in Alzheimer's disease.

Carbonic anhydrase (CA) plays a critical role in pH regulation, long-term synaptic transformation, and is associated with mental retardation, Alzheimer's disease (AD), and Down syndrome. There is accumulating evidence that CAII is increased in AD brain. The present study focused on the determination of CAII protein level in blood plasma samples using immunoblot and ELISA methods.

Caspases-2 and -8 are involved in the presenilin1/gamma-secretase-dependent cleavage of amyloid precursor protein after the induction of apoptosis.

The presenilin/gamma-secretase protease cleaves many type-I membrane proteins, including the amyloid beta-protein (Abeta) precursor (APP). Previous studies have shown that apoptosis induces alterations in Abeta production in a caspase-dependent manner. Here, we report that staurosporine (STS)-induced apoptosis induces caspase-8 and/or-2-dependent gamma-secretase activation.

Structural and functional analyses of minimal phosphopeptides targeting the polo-box domain of polo-like kinase 1.

Polo-like kinase-1 (Plk1) has a pivotal role in cell proliferation and is considered a potential target for anticancer therapy. The noncatalytic polo-box domain (PBD) of Plk1 forms a phosphoepitope binding module for protein-protein interaction. Here, we report the identification of minimal phosphopeptides that specifically interact with the PBD of human PLK1, but not those of the closely related PLK2 and PLK3.

Presenilin 1/gamma-secretase is associated with cadmium-induced E-cadherin cleavage and COX-2 gene expression in T47D breast cancer cells.

Cadmium is a heavy metal that has multiple toxic effects on human health and has been classified as a human carcinogen. E-cadherin is a major target of cadmium; however, the roles of E-cadherin and cadmium and the mechanisms of tumor progression remain to be defined. Here, we demonstrate that cadmium increases E-cadherin processing via a gamma-secretase in the T47D breast cancer cell lines.

Self-regulated Plk1 recruitment to kinetochores by the Plk1-PBIP1 interaction is critical for proper chromosome segregation.

The polo-box domain (PBD) of mammalian polo-like kinase 1 (Plk1) is essential in targeting its catalytic activity to specific subcellular structures critical for mitosis. The mechanism underlying Plk1 recruitment to the kinetochores and the role of Plk1 at this site remain elusive. Here, we demonstrate that a PBD-binding protein, PBIP1, is crucial for recruiting Plk1 to the interphase and mitotic kinetochores.