TMAO enhances TNF-α mediated fibrosis and release of inflammatory mediators from renal fibroblasts.

Trimethylamine-N-oxide (TMAO) is a gut microbiota-derived metabolite and TNF-α is proinflammatory cytokine, both known to be associated with renal inflammation, fibrosis and chronic kidney disease. However, today there are no data showing the combined effect of TMAO and TNF-α on renal fibrosis-and inflammation. The aim of this study was to investigate whether TMAO can enhance the inflammatory and fibrotic effects of TNF-α on renal fibroblasts.

Study of Alzheimer's disease- and frontotemporal dementia-associated genes in the Cretan Aging Cohort.

Using exome sequencing, we analyzed 196 participants of the Cretan Aging Cohort (CAC; 95 with Alzheimer's disease [AD], 20 with mild cognitive impairment [MCI], and 81 cognitively normal controls). The APOE ε4 allele was more common in AD patients (23.2%) than in controls (7.

TMAO Suppresses Megalin Expression and Albumin Uptake in Human Proximal Tubular Cells Via PI3K and ERK Signaling.

Trimethylamine-N-oxide (TMAO) is a uremic toxin, which has been associated with chronic kidney disease (CKD). Renal tubular epithelial cells play a central role in the pathophysiology of CKD. Megalin is an albumin-binding surface receptor on tubular epithelial cells, which is indispensable for urine protein reabsorption.

The Fibrotic Effects of TMAO on Human Renal Fibroblasts Is Mediated by NLRP3, Caspase-1 and the PERK/Akt/mTOR Pathway.

Trimethylamine N-oxide (TMAO), a product of gut microbiota metabolism, has previously been shown to be implicated in chronic kidney disease. A high TMAO-containing diet has been found to cause tubulointerstitial renal fibrosis in mice. However, today there are no data linking specific molecular pathways with the effect of TMAO on human renal fibrosis.

Apolipoprotein E ɛ4 (APOE ɛ4) Allele is Associated with Long Sleep Duration Among Elderly with Cognitive Impairment.

Background: Apolipoprotein E gene (APOE) ɛ4 allele increases the risk for Alzheimer's disease (AD). Furthermore, among patients with cognitive impairment, longer sleep duration is associated with worse cognitive performance. To date, literature examining the associations between APOE ɛ4 allele and objective sleep duration is limited.

Objective Daytime Napping is Associated with Disease Severity and Inflammation in Patients with Mild to Moderate Dementia1.

Background: Patients with dementia report excessive daytime sleep/sleepiness, which is associated with worse cognitive performance. Inflammatory markers may be elevated in patients with dementia and have been proposed as mediators of sleep/sleepiness.

Objective: To examine the association of objective daytime napping with cognitive performance and peripheral markers of inflammation in patients with dementia as compared to not cognitively impaired (NCI) controls.

Associations between sleep duration and cognitive impairment in mild cognitive impairment.

The prevalence of mild cognitive impairment (MCI) increases among elderly people and is associated with a high risk of dementia. Identifying factors that may contribute to the progress of MCI to dementia is critical. The objective of this study was to examine the association of objective sleep with cognitive performance in MCI patients.

The Cretan Aging Cohort: Cohort Description and Burden of Dementia and Mild Cognitive Impairment.

Our aim was to explore the burden of dementia in the Cretan Aging Cohort, comprised of 3140 persons aged ≥60 years (56.8% women, 5.8 ± 3.

Self-reported fatigue as a risk index for dementia diagnosis.

Introduction: Cognitive impairment and frailty are major problems of older age. This study aims to explore the association between frailty and cognitive impairment in a rural cohort of older subjects in southern Europe (Cretan Aging Cohort).

Methods: Community-based, primary care, cross-sectional, study in the Heraklion Prefecture, Crete, Greece.

Potential exposure of humans to Rickettsia felis in Greece.

Rickettsia felis is a flea-transmitted pathogen however, in Greece, much work has been done on another flea-borne pathogen, R. typhi; human cases have been described and high-risk areas have been characterized. Nevertheless, little is known about human infections caused by R.

Linking pesticide exposure and dementia: what is the evidence?

There has been a steep increase in the prevalence of dementia in recent decades, which has roughly followed an increase in pesticide use some decades earlier, a time when it is probable that current dementia patients could have been exposed to pesticides. This raises the question whether pesticides contribute to dementia pathogenesis. Indeed, many studies have found increased prevalence of cognitive, behavioral and psychomotor dysfunction in individuals chronically exposed to pesticides.