98%
921
2 minutes
20
Cognitive decline is frequently seen in patients with chronic kidney disease (CKD). The causes of cognitive decline in these patients are likely to be multifactorial, including vascular disease, uraemic toxins, blood-brain barrier leakage, and metabolic and endocrine changes. Gut dysbiosis is common in patients with CKD and contributes to the increase in uraemic toxins. However, the gut microbiome modulates local and systemic levels of several metabolites such as short-chain fatty acids or derivatives of tryptophan metabolism, neurotransmitters, endocannabinoid-like mediators, bile acids, hormones such as glucagon-like peptide 1 (GLP1) or cholecystokinin (CCK). These factors can affect gut function, immunity, autonomic nervous system activity and various aspects of brain function. Key areas include blood-brain barrier integrity, nerve myelination and survival/proliferation, appetite, metabolism and thermoregulation, mood, anxiety and depression, stress and local inflammation. Alterations in the composition of the gut microbiota and the production of biologically active metabolites in patients with CKD are well documented and are favoured by low-fiber diets, elevated urea levels, sedentary lifestyles, slow stool transit times and polypharmacy. In turn, dysbiosis can modulate brain function and cognitive processes, as discussed in this review. Thus, the gut microbiome may contribute to alterations in cognition in patients with CKD and may be a target for therapeutic interventions using diet, prebiotics and probiotics.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11905753 | PMC |
http://dx.doi.org/10.1093/ndt/gfae253 | DOI Listing |
Alzheimers Dement
September 2025
Department of Public Health, California State University, Fullerton, California, USA.
Introduction: We investigated the associations between diabetes (type 2), hypertension and hypercholesterolemia with mild cognitive impairment (MCI) and Alzheimer's disease (AD) diagnoses by race-ethnicity and sex.
Methods: Data (n = 22,950) were derived via the National Alzheimer's Coordinating Center. Logistic regression was used to assess the relationship between each comorbid condition and MCI and AD.
Alzheimers Dement
September 2025
Multiomics Investigation of Neurodegenerative Diseases (MIND) Lab, Montréal, Québec, Canada.
Living with dementia requires decision making about numerous topics including daily activities and advance care planning (ACP). Both individuals living with dementia and care partners require informed support for decision making. We conducted an umbrella review to assess knowledge translation (KT) interventions supporting decision making for individuals living with dementia and their informal care partners.
View Article and Find Full Text PDFBehav Brain Res
September 2025
Department of neurology, Hebei Medical University Third Hospital, Hebei 050000,Shijiazhuang,China; Hebei Key Laboratory of Neurodegenerative Disease Mechanism, Hebei 050000,Shijiazhuang,China. Electronic address:
Background: Mitochondrial dysfunction is considered to be an important pathogenesis of cognitive impairment in Alzheimer's disease(AD). Activation of Nrf2 can improve cognitive impairment in AD mice, but the underlying mechanism remains to be elucidated. This research aims to investigate the intrinsic molecular mechanism of Nrf2 in mitochondrial biogenesis related to cognitive impairment of AD mice.
View Article and Find Full Text PDFBiol Psychiatry Cogn Neurosci Neuroimaging
September 2025
University of Illinois at Chicago, Department of Psychiatry. Electronic address:
Background: Late-life depression (LLD) is associated with negative outcomes including high rates of recurrence and cognitive decline. However, the neurobiological changes influencing such outcomes in LLD are not well understood. Disequilibrium in large-scale brain networks may contribute to LLD-related cognitive decline.
View Article and Find Full Text PDFNeuropsychologia
September 2025
Icelandic Vision Lab, Department of Psychology, University of Iceland, Saemundargata 2, 102, Reykjavik, Iceland.
Developmental dyslexia is a disorder marked by difficulties in reading, spelling, and connecting sounds to written language. The high-level visual dysfunction hypothesis suggests these difficulties may partially arise from abnormalities in high-level visual cognition such as the ability to integrate visual input for higher-order cognitive functions such as reading. Here we examined adult (mean age = 35) dyslexic readers' neural functioning as they recognized identities of nonlinguistic visual objects, specifically houses and faces.
View Article and Find Full Text PDF