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The medial frontal cortex, including anterior midcingulate cortex, has been linked to multiple psychological domains, including cognitive control, pain, and emotion. However, it is unclear whether this region encodes representations of these domains that are generalizable across studies and subdomains. Additionally, if there are generalizable representations, do they reflect a single underlying process shared across domains or multiple domain-specific processes? We decomposed multivariate patterns of functional MRI activity from 270 participants across 18 studies into study-specific, subdomain-specific, and domain-specific components and identified latent multivariate representations that generalized across subdomains but were specific to each domain. Pain representations were localized to anterior midcingulate cortex, negative emotion representations to ventromedial prefrontal cortex, and cognitive control representations to portions of the dorsal midcingulate. These findings provide evidence for medial frontal cortex representations that generalize across studies and subdomains but are specific to distinct psychological domains rather than reducible to a single underlying process.
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http://dx.doi.org/10.1038/s41593-017-0051-7 | 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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