98%
921
2 minutes
20
The deposition of amyloid-β (Aβ) protein in the human brain is a hallmark of Alzheimer's disease and is related to cognitive decline. However, the relationship between early Aβ deposition and future cognitive impairment remains poorly understood, particularly concerning its spatial distribution and network-level effects. Here, we employed a cross-validated machine learning approach and investigated whether integrating subject-specific brain connectome information with Aβ burden measures improves predictive validity for subsequent cognitive decline. Baseline regional Aβ pathology measures from positron emission tomography (PET) imaging predicted prospective cognitive decline. Incorporating structural connectome, but not functional connectome, information into the Aβ measures improved predictive performance. We further identified a neuropathological signature pattern linked to future cognitive decline, which was validated in an independent cohort. These findings advance our understanding of how Aβ pathology relates to brain networks and highlight the potential of network-based metrics for Aβ-PET imaging to identify individuals at higher risk of cognitive decline.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11661183 | PMC |
http://dx.doi.org/10.1101/2024.12.10.627818 | DOI Listing |
Clin Epigenetics
September 2025
Department of Psychiatry and Psychotherapy, Philipps University Marburg, Marburg, Germany.
Background: Work-related stress is a well-established contributor to mental health decline, particularly in the context of burnout, a state of prolonged exhaustion. Epigenetic clocks, which estimate biological age based on DNA methylation (DNAm) patterns, have been proposed as potential biomarkers of chronic stress and its impact on biological aging and health. However, their role in mediating the relationship between work-related stress, physiological stress markers, and burnout remains unclear.
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 PDFSci Rep
September 2025
Department of Endocrinology, Affiliated Zhongda Hospital of Southeast University, Nanjing, China.
Visceral adiposity has been proposed to be closely linked to cognitive impairment. This cross-sectional study aimed to evaluate the predictive value of Chinese Visceral Adiposity Index (CVAI) for mild cognitive impairment (MCI) in patients with type 2 diabetes mellitus (T2DM) and to develop a quantitative risk assessment model. A total of 337 hospitalized patients with T2DM were included and randomly assigned to a training cohort (70%, n = 236) and a validation cohort (30%, n = 101).
View Article and Find Full Text PDF