Translational research on cognitive impairment in chronic kidney disease DOI
Carsten A. Wagner, Ziad A. Massy, Giovambattista Capasso

et al.

Nephrology Dialysis Transplantation, Journal Year: 2024, Volume and Issue: unknown

Published: Oct. 14, 2024

ABSTRACT Cognitive decline is common in patients with acute or chronic kidney disease. Several areas of brain function can be affected, including short- and long-term memory, attention inhibitory control, sleep, mood, eating control motor function. disease shares risk factors cognitive dysfunction people without disease, such as diabetes, high blood pressure, sedentary lifestyle unhealthy diet. However, additional kidney-specific may contribute, uremic toxins, electrolyte imbalances, inflammation, acid–base disorders endocrine dysregulation. Traditional interact to cause damage the blood–brain barrier, induce vascular neurotoxicity neuroinflammation. Here, we discuss recent insights into pathomechanisms from animal models novel avenues for prevention therapy. We focus on a several that influence cognition: barrier disruption, role skeletal muscle, physical activity factor irisin, emerging therapeutic sodium-glucose cotransporter 2 (SGLT2) inhibitors glucagon-like peptide 1 (GLP-1) receptor agonists. Taken together, these studies demonstrate importance providing mechanistic understanding this complex condition their potential explain mechanisms therapies.

Language: Английский

New-generation antidiabetic medications and dementia risk in older adults with type 2 diabetes: A retrospective cohort study DOI Creative Commons
Avi Cohen, Stephen Z. Levine,

Gabriel Vainstein

et al.

The Journal of Prevention of Alzheimer s Disease, Journal Year: 2025, Volume and Issue: unknown, P. 100199 - 100199

Published: May 1, 2025

New-generation antidiabetic medications may have therapeutic potential for dementia, beyond their glycemic effects. However, information from observational studies exploring the association between new-generation use and dementia risk is limited. To examine medication risk. Retrospective cohort study using electronic health records of a large non-profit maintenance organization. 84,798 dementia-free individuals aged ≥65y with type 2 diabetes. Antidiabetic exposure was based on purchased prescriptions used as time-varying variable. Exposure periods were defined in which either dipeptidyl peptidase-4 inhibitors (DPP-4i), sodium-glucose cotransporter-2 (SGLT-2i), or glucagon-like peptide-1 analogs (GLP-1a) combinations used, otherwise unexposed. Dementia classification International Classification Diseases, Ninth Revision codes antidementia prescriptions. Cox regression models fitted to quantify incident dementia. Models adjusted 13 sources confounding inverse-probability weighting. Among mean diabetes onset age 66.4 ± 7.5 years, median follow-up 8.7 years (Q1-Q3: 5.4-12.8). diagnosed 11,642 (13.7%) individuals. associated reduced (HR = 0.69; 95% CI, 0.66-0.73) by drug classes (DPP-4i, HR 0.67 [95% CI 0.63-0.71]; SGLT-2i, 0.63 0.56-0.70], GLP-1a, 0.61 0.54-0.69]. The results this large-scale suggest that be lower older adults T2D.

Language: Английский

Citations

0

Translational research on cognitive impairment in chronic kidney disease DOI
Carsten A. Wagner, Ziad A. Massy, Giovambattista Capasso

et al.

Nephrology Dialysis Transplantation, Journal Year: 2024, Volume and Issue: unknown

Published: Oct. 14, 2024

ABSTRACT Cognitive decline is common in patients with acute or chronic kidney disease. Several areas of brain function can be affected, including short- and long-term memory, attention inhibitory control, sleep, mood, eating control motor function. disease shares risk factors cognitive dysfunction people without disease, such as diabetes, high blood pressure, sedentary lifestyle unhealthy diet. However, additional kidney-specific may contribute, uremic toxins, electrolyte imbalances, inflammation, acid–base disorders endocrine dysregulation. Traditional interact to cause damage the blood–brain barrier, induce vascular neurotoxicity neuroinflammation. Here, we discuss recent insights into pathomechanisms from animal models novel avenues for prevention therapy. We focus on a several that influence cognition: barrier disruption, role skeletal muscle, physical activity factor irisin, emerging therapeutic sodium-glucose cotransporter 2 (SGLT2) inhibitors glucagon-like peptide 1 (GLP-1) receptor agonists. Taken together, these studies demonstrate importance providing mechanistic understanding this complex condition their potential explain mechanisms therapies.

Language: Английский

Citations

1