Patients with chronic insomnia disorder have increased serum levels of neurofilaments, neuron-specific enolase and S100B: does organic brain damage exist?

Objectives: The aims of this study were to investigate whether serum levels of neurofilaments heavy chain (NfH) and light chain (NfL), neuron-specific enolase (NSE) and S100 calcium binding protein B (S100B): (1) change, (2) alleviate in post-therapy and (3) are associated with sleep quality and cognitive dysfunction, in patients with chronic insomnia disorder (CID).

Methods: Forty CID outpatients constituted free-therapy group (ft-CID), in which twenty-four patients completed follow-up after six-month treatment to form re-visiting group (rv-CID), and twenty healthy good sleepers constituted control group (HC). All subjects completed questionnaires, polysomnography, Chinese-Beijing Version of Montreal Cognitive Assessment (MoCA-C) and Nine Box Maze Test (NBMT) to assess sleep and neuropsychological function.

Age- and Gender-Based Differences in Nest-Building Behavior and Learning and Memory Performance Measured Using a Radial Six-Armed Water Maze in C57BL/6 Mice.

Background: Understanding age-based and gender-based behavioral changes is becoming more important as a greater percentage of people lives longer worldwide. In this study, a C57BL/6 mouse animal model was used to study age-based and gender-based behavioral differences using nest building and radial six-armed water maze (RAWM) testing.

Methods: In C57BL/6 mice, nest-building behavior was recorded as nesting scores, while spatial learning and memory behaviors were assessed using RAWM platform search errors and latencies.

MicroRNA‑126 inhibits endothelial permeability and apoptosis in apolipoprotein E‑knockout mice fed a high‑fat diet.

Endothelial dysfunction and apoptosis have key roles in the initiation and progression of atherosclerosis (AS). AS has been demonstrated to be associated with a high‑fat diet, which may increase endothelial permeability and apoptosis; however, the exact mechanisms underlying the development of AS remain poorly understood. MicroRNAs (miRNAs) are vital for the regulation of cardiovascular disease, and dysregulated miRNAs have been implicated in AS.

Metabolic Effect of 1-Deoxynojirimycin from Mulberry Leaves on db/db Diabetic Mice Using Liquid Chromatography-Mass Spectrometry Based Metabolomics.

Metabolomics was applied to the liquid chromatography-mass spectrometry urinary metabolic profile of type 2 diabetes (T2DM) mice treated with mulberry 1-deoxynojirimycin (DNJ). The serum biochemical indicators related to T2DM like blood glucose, insulin, triglyceride, total cholesterol, nitrogen, malondialdehyde, and creatinine decreased significantly in the treated group. The histopathological changes in liver cells were marked by deformations and disruptions in central area of nuclei in DM mice, whereas DNJ treatment recovered regular liver cells with normal nuclei.

Interferon-γ affects leukemia cell apoptosis through regulating Fas/FasL signaling pathway.

Objective: Imbalance of hematopoietic cell proliferation and apoptosis is one of the major causes of leukemia. Enhanced cell proliferation and reduced apoptosis lead to hemocytes accumulation. Fas/FasL signaling pathway promotes cell apoptosis.

Cognitive Performance and the Alteration of Neuroendocrine Hormones in Chronic Tension-Type Headache.

Tension-type headache (TTH) is the most prevalent primary headache. Chronic TTH (CTTH), the most serious form of TTH, is refractory, with a high socio-economic burden. Research studies have shown patients with migraine often had cognitive impairment, but few studies have focused on the cognition in patients with CTTH.

Research Progress on the Risk Factors and Outcomes of Human Carotid Atherosclerotic Plaques.

Objective: Atherosclerosis is an inflammatory process that results in complex lesions or plaques that protrude into the arterial lumen. Carotid atherosclerotic plaque rupture, with distal atheromatous debris embolization, causes cerebrovascular events. This review aimed to explore research progress on the risk factors and outcomes of human carotid atherosclerotic plaques, and the molecular and cellular mechanisms of human carotid atherosclerotic plaque vulnerability for therapeutic intervention.

Accelerated reduction of serum thyroxine and hippocampal histone acetylation links to exacerbation of spatial memory impairment in aged CD-1 mice pubertally exposed to bisphenol-a.

Age-related cognitive decline has been associated with changes in endogenous hormones and epigenetic modification of chromatin, including histone acetylation. Developmental exposure to endocrine disrupting chemicals, such as bisphenol-A (BPA) that produces endocrine disruption and epigenetic changes, may be a risk factor for accelerating cognitive deficits during aging. Thus, we exposed CD-1 mice to BPA (0, 1, and 100 mg/l BPA in the drinking water) orally during puberty (from postnatal days 28 to 56) and investigated whether pubertal BPA exposure exacerbates the age-related impairment of spatial cognition in old age (18 months old) and whether serum sex and thyroid hormones or hippocampal histone acetylation (H3K9ac and H4K8ac) are associated with cognitive effects.

Inflammatory insult during pregnancy accelerates age-related behavioral and neurobiochemical changes in CD-1 mice.

Data shows that inflammation during pregnancy significantly exerts a long-term influence on offspring, such as increasing the risk of adult cognition decline in animals. However, it is unclear whether gestational inflammation affects the neurobehavioral and neurobiochemical outcomes in the mother-self during aging. In this study, pregnant CD-1 mice intraperitoneally received lipopolysaccharide (LPS) in two doses (25 and 50 g/kg, respectively) or normal saline daily during gestational days 15-17.

Maternal inflammation linearly exacerbates offspring age-related changes of spatial learning and memory, and neurobiology until senectitude.

Maternal inflammation during pregnancy can elevate the risk of neurodegenerative disorders in offspring. However, how it affects age-related impairments of spatial learning and memory and changes in the neurobiological indictors in the offspring in later adulthood is still elusive. In this study, the CD-1 mice with maternal gestational inflammation due to receiving lipopolysaccharide (LPS, i.

Chronic adjunction of 1-deoxynojirimycin protects from age-related behavioral and biochemical changes in the SAMP8 mice.

Several studies have indicated that a caloric restriction mimetic or treatment for type 2 diabetes may reverse brain aging. Therefore, we investigated the effect of 1-deoxynojirimycin (DNJ), an alkaloid acting as an inhibitor of α-glucosidase, on age-related behavioral and biochemical changes. SAMP8 mice were randomly assigned to a control group labeled "old" or to the 10- or 20-mg/kg/day DNJ groups.

Hippocampal synaptotagmin-4 is correlated with impaired spatial learning and memory in SAMP8 mice.

The mechanism underlying age-related cognitive impairment remains unclear. To determine whether synaptotagmin (Syt)-1 and Syt-4 are involved in age-related cognitive impairment, we used a radial six-arm water maze (RAWM) to evaluate spatial learning and memory deficits in the senescence accelerated prone mouse 8. The Syt-1 and Syt-4 levels of different subregions of the dorsal hippocampus (DH) were detected through immunohistochemistry.

Myosin light chain kinase inhibitor ML7 improves vascular endothelial dysfunction via tight junction regulation in a rabbit model of atherosclerosis.

Vascular endothelial dysfunction (VED) is an important factor in the initiation and development of atherosclerosis (AS). Previous studies have demonstrated that endothelial permeability is increased in diet‑induced AS. However, the precise underlying mechanisms remain poorly understood.

Melatonin alleviates myosin light chain kinase expression and activity via the mitogen-activated protein kinase pathway during atherosclerosis in rabbits.

Melatonin (MLT) is an endogenous indole compound with numerous biological activities that has been associated with atherosclerosis (AS). In the present study, rabbits were used as an AS model in order to investigate whether MLT affects endothelial cell permeability, myosin light chain kinase (MLCK) activity and MLCK expression via the mitogen-activated protein kinase (MAPK) pathway. Expression and activity of MLCK were measured using western blot analysis, quantitative polymerase chain reaction, immunohistochemistry and γ-32P-adenosine triphosphate incorporation.