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Background: While many studies have suggested that heart failure (HF) may lead to cognitive impairment, our understanding about this relationship is limited. This study investigated the association of cognitive function with HF risk factors and how cognitive impairment may impact the development of incident clinical HF in people with subclinical HF.
Methods: People with either preclinical (at risk and asymptomatic, n=814) or clinical (symptomatic, n=1152) HF were recruited from communities, clinics, and hospitals in 5 Australian states (Victoria, New South Wales, South Australia, Tasmania, and Queensland). Cognitive impairment was measured with the Montreal Cognitive Assessment (MOCA <26). Left ventricular dysfunction was assessed as global longitudinal strain (<16%). Patients with preclinical HF were followed up for 45±13 months for incident clinical HF or death.
Results: Baseline MOCA was independently associated with age, HF stage, diabetes, atrial fibrillation, chronic lung disease, cerebrovascular disease, global longitudinal strain, left atrial volume index, and left ventricular filling pressure. Cognitive impairment significantly increased the associations of age (interaction <0.001), comorbidity index (interaction<0.001), and global longitudinal strain (interaction =0.042) with clinical HF. Of patients with preclinical HF at baseline, 71 (9%) developed clinical HF and 87 (11%) died within the follow-up period. In time-to-event analysis of participants with preclinical HF, those with either cognitive impairment or left ventricular dysfunction had double the risk of developing clinical HF, compared with those with normal cognition and left ventricular function. Those with concomitant cognitive impairment and left ventricular dysfunction had a 4-fold greater risk of developing HF (subdistribution hazard ratio, 4.01 [95% CI, 2.39-6.76]).
Conclusions: Cognitive impairment is associated with increased risk of incident clinical HF, independent of cardiac function and other HF risk factors.
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http://dx.doi.org/10.1161/JAHA.124.039697 | DOI Listing |
Psychopharmacology (Berl)
September 2025
División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Ciudad Universitaria, Mexico City, 04510, Mexico.
Rationale: One of the earliest changes associated with Alzheimer's disease (AD) is the loss of catecholaminergic terminals in the cortex and hippocampus originating from the Locus Coeruleus (LC). This decline leads to reduced catecholaminergic neurotransmitters in the hippocampus, affecting synaptic plasticity and spatial memory. However, it is unclear whether restoring catecholaminergic transmission in the terminals from the LC may alleviate the spatial memory deficits associated with AD.
View Article and Find Full Text PDFNaunyn Schmiedebergs Arch Pharmacol
September 2025
Pharmacology and Toxicology Department, Faculty of Pharmacy and Biotechnology, German University in Cairo, Gamal Abdel Nasser, 11835, New Cairo, Egypt.
Licochalcone A (LCA), a natural flavonoid with potent anti-inflammatory properties, has shown promise as a neuroprotective agent. However, its ability to cross the blood-brain barrier (BBB) and exert central effects remains underexplored. In this study, we demonstrate for the first time that LCA enhances cognitive function in a lipopolysaccharide (LPS)-induced neuroinflammatory mouse model and effectively penetrates the BBB.
View Article and Find Full Text PDFNeurol Res
September 2025
Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran.
Objectives: This study aimed to investigate the effects of repeated exposure to sevoflurane as an anesthetic agent during various developmental stages, namely neonatal, preadolescent, and adult, on behavioral, synaptic, and neuronal plasticity in male and female Wistar rats.
Methods: Rats were exposed to sevoflurane during three developmental stages: neonatal (PN7), pre-adolescence (PN28), and adulthood (PN90). Behavioral performance was evaluated with the Morris Water Maze.
Radiology
September 2025
Department of Radiology and Radiological Sciences, Johns Hopkins University, Baltimore, Md.
Background Elevated brain iron is a potential marker for neurodegeneration, but its role in predicting onset of mild cognitive impairment (MCI) and prospective cognitive trajectories remains unclear. Purpose To investigate how brain iron and amyloid-β (Aβ) levels, measured using quantitative susceptibility mapping (QSM) MRI and PET, help predict MCI onset and cognitive decline. Materials and Methods In this prospective study conducted between January 2015 and November 2022, cognitively unimpaired older adults underwent baseline QSM MRI.
View Article and Find Full Text PDFRadiology
September 2025
Boston University, VA Boston Health Care System, Boston Medical Center, One Boston Medical Center Place, Boston, MA 02118.