Interactive association between insomnia symptoms and sleep duration for the risk of dementia-a prospective study in the Swedish National March Cohort.

Objective: Given the importance of sleep in maintaining neurocognitive health, both sleep duration and quality might be component causes of dementia. However, the possible role of insomnia symptoms as risk factors for dementia remain uncertain.

Methods: We prospectively studied 22,078 participants in the Swedish National March Cohort who were free from dementia and stroke at baseline.

Influence of chronic diseases on the occurrence of depression: A 13-year follow-up study from the Survey of Health, Ageing and Retirement in Europe.

The causal association between chronic diseases and depression remains unclear. This study aimed to explore the effects of types and number of chronic diseases on the risk of depression using data from the Survey of Health, Ageing and Retirement in Europe (SHARE). A self-admitted questionnaire was used to obtain data on 14 predefined chronic diseases and the European-Depression Scale (EURO-D) was used to assess depression.

Work-Related Stress and Occurrence of Cardiovascular Disease: A 13-Year Prospective Study.

Objective: The aim of the study is to investigate the influence of work-related psychological and physical stresses on risk of cardiovascular disease (CVD).

Methods: A total of 5651 CVD-free participants older than 50 years from the Survey of Health, Ageing and Retirement in Europe were followed up for 13 years to detect incident CVD. Work-related stress was assessed using job strain and job reward questionnaire.

Working life job strain status and cognitive aging in Europe: A 12-year follow-up study.

Background: To examine the association of job strain with cognitive ability and the influence of life-course job strain on later life cognitive decline.

Methods: Data were derived from six waves of the Survey of Health, Aging, and Retirement in Europe. The study sample consists of 13349 participants aged 50 to 98 years at wave 2 and has been followed up for 12-years.

Depressive symptoms and cognitive impairment: A 10-year follow-up study from the Survey of Health, Ageing and Retirement in Europe.

Background: Depressive symptoms and cognitive impairment often coexisted in the elderly. This study investigates the effect of late-life depressive symptoms on risk of mild cognitive impairment (MCI).

Methods: A total of 14,231 dementia- and MCI free participants aged 60+ from the Survey of Health, Ageing, and Retirement in Europe were followed-up for 10 years to detect incident MCI.

The relationship between chronic diseases and depression in middle-aged and older adults: A 4-year follow-up study from the China Health and Retirement Longitudinal Study.

Background: Evidence of the association between common chronic diseases and depression is sparse.

Methods: Totally 7819 participants aged 45+ without depression at baseline were followed-up (2011-2015) to detect incident depression. Chronic diseases and depression were defined by self-reported diagnosis and the Center for Epidemiological Studies Depression Scale (CES-D10), respectively.

Late-life depression and the risk of dementia in 14 countries: a 10-year follow-up study from the Survey of Health, Ageing and Retirement in Europe.

Background: Depression is the most common mental health problem and often co-occurs with dementia in old age. This study investigates the influence of late-life depression on risk of dementia.

Methods: A total of 16210 dementia-free participants aged 60+ from the Survey of Health, Aging, and Retirement in Europe were followed up for 10 years to detect incident dementia.

Targetting Exosomes as a New Biomarker and Therapeutic Approach for Alzheimer's Disease.

Alzheimer's disease (AD) is a neurodegenerative disease that mainly occurs in old age and involves progressive cognitive impairment. AD has become a major global issue for public health, with approximately 24 million people currently affected by the disease. Estimates indicted that this number will quadruple by 2050.

Reciprocal associations between job strain and depression: A 2-year follow-up study from the Survey of Health, Ageing and Retirement in Europe.

Background: A growing number of people suffered from depression. This study examined the depression prevalence in workers across 10 European countries plus Israel and the reciprocal associations between job strain and depression.

Methods: The study population consisted of 7,879 workers aged 50-63 years at baseline (2004) from the Survey of Health, Ageing, and Retirement in Europe (SHARE).

Reciprocal relationship between psychosocial work stress and quality of life: the role of gender and education from the longitudinal study of the Survey of Health, Ageing and Retirement in Europe.

Objective: To investigate the reciprocal relationship between psychosocial work stress and quality of life (QoL) and to examine whether the relationship can be moderated by gender or education.

Design: Longitudinal, population-based study.

Setting: The Survey of Health, Ageing and Retirement in Europe (SHARE).

High glucose induces formation of tau hyperphosphorylation via Cav-1-mTOR pathway: A potential molecular mechanism for diabetes-induced cognitive dysfunction.

The abnormally hyperphosphorylated tau is thought to be implicated in diabetes-associated cognitive deficits. The role of mammalian target of rapamycin (mTOR) / S6 kinase (S6K) signalling in the formation of tau hyperphosphorylation has been previously studied. Caveolin-1 (Cav-1), the essential structure protein of caveolae, promotes neuronal survival and growth, and inhibits glucose metabolism.

Elevations in the Levels of NF-κB and Inflammatory Chemotactic Factors in the Brains with Alzheimer's Disease - One Mechanism May Involve α3 Nicotinic Acetylcholine Receptor.

The purpose of this study was to investigate the alterations in the levels of nuclear factor κBp65 (NF-κBp65), monocyte chemoattractant protein 1 (MCP-1/CCL-2) and macrophage inflammatory protein 1α (MIP-1α/CCL-3) in relationship to the expression of α3 nicotinic acetylcholine receptor (nAChR) during the pathogenesis of Alzheimer's disease (AD). The post-mortem human brains of AD and age-matched control individuals, SH-SY5Y and U87MG cell lines exposed to β-amyloid peptide (Aβ), as well as the SH-SY5Y cells in which α3 nAChR was down-regulated by siRNA were used to study the possible expression changes of the targets such as NF-κBp65, MCP-1, MIP-1α and α3 nAChR. The immunohistochemistry results showed the increased immunoreactivities of NF-κBp65, MCP-1 and MIP-1α in neurons in hippocampal and temporal and frontal regions of AD brains.

Original Research: Influence of okadaic acid on hyperphosphorylation of tau and nicotinic acetylcholine receptors in primary neurons.

The aim of the study was to investigate the influence of hyperphosphorylation of tau induced by okadaic acid on the expression of nicotinic acetylcholine receptors and the neurotoxicity of β-amyloid peptide. Primary cultures of neurons isolated from the hippocampus of the brains of neonatal rats were exposed to okadaic acid or/and Aβ1-42 Tau phosphorylated at Ser404 and Ser202, and the protein expressions of α7, α4 and α3 nAChR subunits were quantified by Western blotting, and their corresponding mRNAs by real-time PCR. Superoxide dismutase activity was assayed biochemically and malondialdehyde by thiobarbituric acid-reactive substance.

Comparison of Various Types of Ligand Decorated Nanoliposomes for their Ability to Inhibit Amyloid Aggregation and to Reverse Amyloid Cytotoxicity.

Three different amyloid targeting ligands, previously shown to exhibit amyloid specific properties, have been used to develop amyloid -targeted nanoliposomes (AT-NLs. For this a MAb against Aβ-peptides (Aβ-MAb (immobilized on NLs at 0.015 and 0.

mTor mediates tau localization and secretion: Implication for Alzheimer's disease.

Abnormally hyperphosphorylated tau aggregates form paired helical filaments (PHFs) in neurofibrillary tangles, a key hallmark of Alzheimer's disease (AD) and other tauopathies. The cerebrospinal fluid (CSF) levels of soluble total tau and phospho-tau from clinically diagnosed AD patients are significantly higher compared with controls. Data from both in vitro and in vivo AD models have implied that an aberrant increase of mammalian target of rapamycin (mTor) signaling may be a causative factor for the formation of abnormally hyperphosphorylated tau.

Repeated intraperitoneal injections of liposomes containing phosphatidic acid and cardiolipin reduce amyloid-β levels in APP/PS1 transgenic mice.

Unlabelled: The accumulation of extracellular amyloid-beta (Aβ) peptide and intracellular neurofibrillary tangles in the brain are two major neuropathological hallmarks of Alzheimer's disease (AD). It is thought that an equilibrium exists between Aβ in the brain and in the peripheral blood and thus, it was hypothesized that shifting this equilibrium towards the blood by enhancing peripheral clearance might reduce Aβ levels in the brain: the 'sink effect'. We tested this hypothesis by intraperitoneally injecting APP/PS1 transgenic mice with small unilamellar vesicles containing either phosphatidic acid or cardiolipin over 3weeks.

Lycopene attenuates insulin signaling deficits, oxidative stress, neuroinflammation, and cognitive impairment in fructose-drinking insulin resistant rats.

Fructose intake is linked with the increasing prevalence of insulin resistance, and insulin resistance links Alzheimer's disease with impaired insulin signaling, oxidative damage, neuroinflammation, and cognitive impairment. As a member of the carotenoid family of phytochemicals, lycopene is used as a potent free scavenger, and has been demonstrated to be effective in anti-oxidative stress and anti-inflammatory reaction in the models of AD and other neurodegenerative diseases. Here, we investigated the effect of lycopene on learning and memory impairment and the possible underlying molecular events in fructose-drinking insulin resistant rats.

The decreased expression of mitofusin-1 and increased fission-1 together with alterations in mitochondrial morphology in the kidney of rats with chronic fluorosis may involve elevated oxidative stress.

This study was designed to characterize changes in the expression of mitofusin-1 (Mfn1) and fission-1 (Fis1), as well as in mitochondrial morphology in the kidney of rats subjected to chronic fluorosis and to elucidate whether any mitochondrial injury observed is associated with increased oxidative stress. Sixty Sprague-Dawley (SD) rats were divided randomly into 3 groups of 20 each, i.e.

mTor is a signaling hub in cell survival: a mass-spectrometry-based proteomics investigation.

mTor plays a central role in controlling protein homeostasis and cell survival. Recently, we have demonstrated that perturbations of mTor signaling are implicated in Alzheimer's disease (AD) and that mTor complex 1 (mTorC1) is involved in the formation of toxic phospho-tau. Therefore, we employed mass-spectrometry-based proteomics to identify specific protein expression changes in relation with cell survival in human neuroblastoma SH-SY5Y cells expressing genetically modified mTor.

Dementia studies in Chinese populations.

Variations in the prevalence of dementia in different ethnic groups have been reported worldwide, and a number of reviews have provided a picture of epidemiological studies in dementia research. However, little is known about epidemiological studies in Chinese populations. In this review, we searched PubMed and the Web of Science for original research articles published in English up to July 2013 on the prevalence, incidence, risk factors, and prognosis of dementia in Chinese populations worldwide.

A lifespan observation of a novel mouse model: in vivo evidence supports aβ oligomer hypothesis.

Transgenic mouse models are powerful tools in exploring the mechanisms of AD. Most current transgenic models of AD mimic the memory impairment and the main pathologic features, among which the formation of beta-amyloid (Aβ) plaques is considered a dominant pathologic event. Recently, Aβ oligomers have been identified as more neurotoxic than Aβ plaques.

Dysregulated mTOR-dependent signaling in neurodegeneration or carcinogenesis: implication for Alzheimer's disease and brain tumors.

Recent evidence implicated aberrant mammalian target of rapamycin (mTOR)-dependent signaling in both Alzheimer's disease (AD) and brain tumors. This review focuses on the potential mechanisms shared by both neurodegeneration and carcinogenesis. In particular, attention was paid to the possible roles of mTOR-dependent signaling in these two fundamental pathophysiological processes.

Mammalian target of rapamycin (mTor) mediates tau protein dyshomeostasis: implication for Alzheimer disease.

Previous evidence from post-mortem Alzheimer disease (AD) brains and drug (especially rapamycin)-oriented in vitro and in vivo models implicated an aberrant accumulation of the mammalian target of rapamycin (mTor) in tangle-bearing neurons in AD brains and its role in the formation of abnormally hyperphosphorylated tau. Compelling evidence indicated that the sequential molecular events such as the synthesis and phosphorylation of tau can be regulated through p70 S6 kinase, the well characterized immediate downstream target of mTor. In the present study, we further identified that the active form of mTor per se accumulates in tangle-bearing neurons, particularly those at early stages in AD brains.

Pioglitazone improves cognitive function via increasing insulin sensitivity and strengthening antioxidant defense system in fructose-drinking insulin resistance rats.

Insulin resistance (IR) links Alzheimer's disease (AD) with oxidative damage, cholinergic deficit, and cognitive impairment. Peroxisome proliferator-activated receptor γ (PPARγ) agonist pioglitazone previously used to treat type 2 diabetes mellitus (T2DM) has also been demonstrated to be effective in anti-inflammatory reaction and anti-oxidative stress in the animal models of AD and other neuroinflammatory diseases. Here, we investigated the effect of pioglitazone on learning and memory impairment and the molecular events that may cause it in fructose-drinking insulin resistance rats.