S-ketamine alleviates depression-like behavior and hippocampal neuroplasticity in the offspring of mice that experience prenatal stress.

Prenatal stress exerts long-term impact on neurodevelopment in the offspring, with consequences such as increasing the offspring's risk of depression in adolescence and early adulthood. S-ketamine can produce rapid and robust antidepressant effects, but it is not clear yet whether and how S-ketamine alleviates depression in prenatally stressed offspring. The current study incestigated the preliminary anti-depression mechanism of S-ketamine in prenatally stressed offspring, particularly with regard to neuroplasticity.

Hippocampal Crhr1 conditional gene knockout ameliorated the depression-like behavior and pathological damage in male offspring mice caused by chronic stress during pregnancy.

Numerous studies have demonstrated that chronic stress during pregnancy (CSDP) can induce depression and hippocampal damage in offspring. It has also been observed that high levels of corticotropin-releasing hormone (CRH) can damage hippocampal neurons, and intraperitoneal injection of a corticotropin releasing hormone receptor 1 (CRHR1) antagonist decreases depression-like behavior and hippocampal neuronal damage in a mouse depression model. However, whether CSDP causes hippocampal damage and depression in offspring through the interaction of CRH and hippocampal CRHR1 remains unknown and warrants further investigation.

CSF sAPPα and sAPPβ levels in Alzheimer's Disease and Multiple Other Neurodegenerative Diseases: A Network Meta-Analysis.

The soluble amyloid protein procurer α (sAPPα) and β (sAPPβ) have been postulated as promising new cerebrospinal fluid (CSF) biomarkers for Alzheimer's disease (AD) and multiple other neurodegenerative diseases, but have failed to meet expectations with their often discordant and even contradictory findings to date. The aim of the study was to systematically explore this issue. Cochrane Library, PubMed, and CNKI were systematically searched without language or date restrictions.

The Synergistic Roles of the Chronic Prenatal and Offspring Stress Exposures in Impairing Offspring Learning and Memory.

In Alzheimer's disease (AD), extensive experimental studies have demonstrated a negative impact of chronic stress during various stages of life (including prenatal phase) on some aspects of AD pathology. Nevertheless, presently, few studies have been involved in the learning and memory impairments, as well as neuropathology elicited by the chronic prenatal stress (CPS) and the chronic offspring stress (COS) exposures simultaneously, particularly for the adult male APPswe/PS1dE9 murine offspring. Therefore, the aim of the present study was to investigate the influence of CPS on learning and memory impairments induced by COS in 6-month-old male APPswe/PS1dE9 offspring mice and the related mechanism.

Use of CSF α-synuclein in the differential diagnosis between Alzheimer's disease and other neurodegenerative disorders.

Background: The etiology and pathogenesis of neurodegenerative disorders has yet to be elucidated, so their differential diagnosis is a challenge. This is especially true in differentiating Alzheimer's disease (AD), dementia with Lewy bodies (DLB), Parkinson disease (PD), and multiple system atrophy (MSA).

Methods: A total of 11 eligible articles were identified by search of electronic databases including PubMed, Springer Link, Elsevier, and the Cochrane Library, up to June 2014.

Assessment of CSF Aβ42 as an aid to discriminating Alzheimer's disease from other dementias and mild cognitive impairment: a meta-analysis of 50 studies.

Mild Alzheimer's disease (AD) is usually difficult to differentiate from other dementias or mild cognitive impairment (MCI). The aim of our study is to evaluate the clinical importance of cerebrospinal fluid (CSF) β-amyloid 42 (Aβ42) in MCI, AD and other dementias, more specifically: frontotemporal dementia (FTD), dementia with Lewy bodies (DLB), Parkinson's disease (PD) with dementia (PDD) and vascular dementia (VaD). Fifty eligible articles were identified by search of databases including PubMed, EMBASE, Elsevier, Springer Link and the Cochrane Library, from January 1990 to May 2014.

Does CSF p-tau181 help to discriminate Alzheimer's disease from other dementias and mild cognitive impairment? A meta-analysis of the literature.

To evaluate the clinical importance of cerebrospinal fluid (CSF) phosphorylated tau 181 (p-tau181) in mild cognitive impairment (MCI), Alzheimer's disease (AD) and other dementias, more specifically: frontotemporal degeneration (FTD), dementia with Lewy bodies (DLB), vascular dementia (VaD) and Parkinson's disease (PD) with dementia (PDD). Fifty eligible articles were identified by search of databases including PubMed, EMBASE, Elsevier, Springer Link and the Cochrane Library, up to December 2013. The random effects model was used to calculate the standardized mean difference (SMD) with corresponding 95% CI by STATA 9.

[Impact of evening exercise on college students' sleep quality].

Objective: To investigate the impact of college students' evening exercise on their sleep quality, so as to provide a scientific basis for college students to choose an appropriate method of exercise and improve their sleep quality.

Methods: From September to October in 2012, Multi-stage cluster random sampling method was used to select the 5997 college students in Anhui province. The status of college students' exercise and their sleep quality were investigated by the general situation questionnaire, Physical activity rating scale-3(PARS-3), Rating of perceived exertion(RPE) and Pittsburgh sleep quality index(PSQI).

Protective effects of astragalosides on dexamethasone and Aβ25-35 induced learning and memory impairments due to decrease amyloid precursor protein expression in 12-month male rats.

Alzheimer's disease (AD) is a chronic neurodegenerative disorder of the elderly characterized by learning and memory impairment. Stress level glucocorticoids (GCs) and β-amyloid (Aβ) peptide deposition are found to be correlated with dementia progression in patients with AD. The astragalosides (AST) was extracted from traditional Chinese herb Astragalus membranaceous.

Dexamethasone and Aβ₂₅-₃₅ accelerate learning and memory impairments due to elevate amyloid precursor protein expression and neuronal apoptosis in 12-month male rats.

Alzheimer's disease (AD) is an irreversible, progressive brain disorder of the elderly characterized by learning and memory impairment. Stress level glucocorticoids (GCs) and β-amyloid (Aβ) peptides deposition are found to be correlated with dementia progression in patients with AD. However, little is known about the simultaneous effects of glucocorticoids and Aβ on learning and memory impairment and its mechanism.

Dexamethasone potentiated Aβ-induced learning and memory impairment in rats.

Objective: To determine whether dexamethasone (DEX) could potentiate amyloid beta-protein (Abeta)-induced learning and memory impairment in rats, and, if so, what the underlying mechanism is.

Methods: Morris water maze was used to investigate whether DEX could potentiate Abeta-induced learning and memory impairment in rats, and the histopathologic changes in CA1 field of hippocampus were examined under a light microscope. Immunohistochemistry was used to observe the change of the phosphorylated tau at Thr-231 in the CA1 field of hippocampus.

Glucocorticoids increase impairments in learning and memory due to elevated amyloid precursor protein expression and neuronal apoptosis in 12-month old mice.

Alzheimer's disease is a chronic neurodegenerative disorder marked by a progressive loss of memory and cognitive function. Stress level glucocorticoids are correlated with dementia progression in patients with Alzheimer's disease. In this study, twelve month old male mice were chronically treated for 21 days with stress-level dexamethasone (5mg/kg).

Memory and learning impairment induced by dexamethasone in senescent but not young mice.

In this study, the memory and learning impairment induced by dexamethasone in young mice and senescent mice were evaluated by step-down inhibitory avoidance task and passive avoidance test. Colorimetric MTT(tetrazole 3-(4,5-dimethylthiazol-2-yl-)-2,5-diphenyltetrazolium bromide) assay and TUNEL staining were used to investigate the influence of dexamethasone on hippocampal neuronal cell death with amyloid beta-protein. It was determined the effect of dexamethasone on intracellular calcium ([Ca(2+)](i)) with amyloid beta-protein 25-35 by fluorescence imaging with a confocal laser microscope using fluo-3 acetoxymethylester (AM) as a fluorescent dye.