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Vagally mediated heart rate variability (vmHRV) at resting state has been associated to cognitive functions dependent on cognitive control, such as memory. However, little is known about the phasic interaction between cognitive and autonomic control. In a pre-registered within-between-subject designed experiment, the potential of vmHRV biofeedback to simultaneously stimulate vmHRV during memory processing and cognitive control over long-term memory was tested, along with investigating psychophysiological association. 71 young healthy adults completed (twice) a false memory task in virtual reality. Immediately before memory encoding and retrieval, participants practiced either vmHRV biofeedback or a control breathing exercise. Cognitive control over long-term memory was assessed as the confidence toward false memories and the capability to discriminate them from true memories. Resting-state vmHRV before each test and phasic vmHRV during memory encoding and retrieval were measured as the root mean square differences (RMSSD) in the heart period. vmHRV biofeedback had neither an immediate effect on measures of cognitive control over long-term memory nor on phasic RMSSD. Moreover, neither resting-state nor phasic vmHRV correlated to the cognitive scores. Consequently, the utility of HRV biofeedback as a psychophysiological stimulation tool and a link between vmHRV and cognitive control over long-term memory could not be verified. Exploratory analyses revealed that baseline shift in parasympathetic activity confounded the psychophysiological association. Future directions are provided that could shed light on the relationship between cognition and vmHRV.
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http://dx.doi.org/10.1111/psyp.14588 | DOI Listing |
Alzheimers Res Ther
September 2025
Department of Neurology, Saarland University, Kirrberger Straße, 66421, Homburg/Saar, Germany.
Background: Alzheimer's disease (AD) patients and animal models exhibit an altered gut microbiome that is associated with pathological changes in the brain. Intestinal miRNA enters bacteria and regulates bacterial metabolism and proliferation. This study aimed to investigate whether the manipulation of miRNA could alter the gut microbiome and AD pathologies.
View Article and Find Full Text PDFAlzheimers Dement
September 2025
Department of Neurology, University of Michigan, Ann Arbor, Michigan, USA.
Introduction: Mild cognitive impairment (MCI) represents a transitional stage between normal aging and dementia. We investigate associations among cardiovascular and metabolic disorders (hypertension, diabetes mellitus, and hyperlipidemia) and diagnosis (normal; amnestic [aMCI]; and non-amnestic [naMCI]).
Methods: Multinomial logistic regressions of participant data (N = 8737; age = 70.
J Mol Neurosci
September 2025
Department of Physiology, School of Medicine, Dokuz Eylul University, Izmir, Turkey.
The ketogenic diet (KD), a high-fat, low-carbohydrate regimen, has been shown to exert neuroprotective effects in various neurological models. This study explored how KD-alone or combined with antibiotic-induced gut microbiota depletion-affects cognition and neuroinflammation in aging. Thirty-two male rats (22 months old) were assigned to four groups (n = 8): control diet (CD), ketogenic diet (KD), antibiotics with control diet (AB), and antibiotics with KD (KDAB).
View Article and Find Full Text PDFGeroscience
September 2025
Department of Neurology, Albert Einstein College of Medicine, Bronx, NY, USA.
Cognitive decline is common in multiple sclerosis (MS), although neural mechanisms are not fully understood. The objective was to investigate the impact of mild cognitive impairment (MCI) on the relationship between resting state functional connectivity (RSFC) and cognitive function in older adults with multiple sclerosis (OAMS) and age matched healthy controls. Participants underwent magnetic resonance imaging (MRI) scans and cognitive assessments.
View Article and Find Full Text PDFNat Commun
September 2025
Institute of Neurosciences and Medicine, Brain & Behaviour (INM-7), Research Centre Juelich; Wilhelm-Johnen-Straße 1, Juelich, Germany.
Autism is a neurodevelopmental condition associated with altered resting-state brain function. An increased excitation-inhibition ratio is discussed as a pathomechanism but in-vivo evidence of disturbed neurotransmission underlying functional alterations remains scarce. We compare local resting-state brain activity and neurotransmitter co-localizations between autism (N = 405, N = 395) and neurotypical controls (N = 473, N = 474) in two independent cohorts and correlate them with excitation-inhibition changes induced by glutamatergic (ketamine) and GABAergic (midazolam) medication.
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