ArticleProceedings of the National Academy of Sciences of the United States of America2022
Amyloid-β and tau pathologies relate to distinctive brain dysconnectomics in preclinical autosomal-dominant Alzheimer's disease.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed.
- APOE4-AGE axis is linked to mtDNA release and cGAS-STING-mediated neuroinflammation in the aging brain.Free radical biology & medicine · 2026Article
- Diurnal dynamics of multilayer brain networks predict cognitive trajectories in aging.GeroScience · 2026Article
- Amygdalar Pattern Similarity to Negative and Neutral Images, Ratings of the Images, and PET-Measured Amyloid and Tau Levels in Older Adults Without Dementia.Affective science · 2026Article
- Aberrant large- and mesoscale network segregation and integration in bulimia nervosa.Journal of eating disorders · 2026Article
- Hierarchical organization of tau topography across the Alzheimer's disease continuum integrates amyloid, connectome, and intrinsic molecular vulnerability.Communications biology · 2026Article
- Non-linear associations of amyloid-β with resting-state functional networks and their cognitive relevance in a large community-based cohort of cognitively normal older adults.Alzheimer's research & therapy · 2026Article
- Precise Aβ clearance and antioxidant therapy in Alzheimer's disease via photoacoustic imaging-guided palladium hydride nanosheet-mediated photothermal treatment.BMC neuroscience · 2026Article
- Engram cell vulnerability in neurodegeneration: from mechanistic insights to therapeutic horizons.Frontiers in aging neuroscience · 2026Review
- Subregional Functional Connectivity of the Precuneus as a Preclinical Biomarker in Alzheimer's Disease.Neurology research international · 2026Article
- Pretangle tau pathology accrual in the default mode network during the progression of Alzheimer's disease.Molecular neurodegeneration advances · 2026Article
- Contribution of local amyloid-β and tau burden to hypometabolism in autosomal-dominant Alzheimer's disease.Brain communications · 2026Article
- Material-based neuroimaging and biomarker detection for central nervous system disorder.Materials today. Bio · 2025Review
- Article
- Abnormal Brain Iron Metabolism is Linked to Altered Neural Function in Isolated Laryngeal Dystonia.Movement disorders : official journal of the Movement Disorder Society · 2025Article
- Tau-PET pathology in the subregions of the amygdala and its associations with cognitive performance and neuropsychiatric symptoms in autosomal dominant Alzheimer's disease.Alzheimer's research & therapy · 2025Article
- Driving research on successful aging and neuroprotection in Latin America: Insights from the inaugural symposium on brain resilience and healthy longevity.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Connectome-based predictive modeling of brain pathology and cognition in autosomal dominant Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Heterogeneous brain abnormalities in subjective cognitive decline converge on a common network and their transcriptional signature.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Hyperconnectivity and Connectome Gradient Dysfunction of Cerebello-Thalamo-Cortical Circuitry in Alzheimer's Disease Spectrum Disorders.Cerebellum (London, England) · 2025Article
- Hippocampal Subfield Volume in Relation to Cerebrospinal Fluid Amyloid-ß in Early Alzheimer's Disease: Diagnostic Utility of 7T MRI.European journal of neurology · 2025Article
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12 authors.
Funding
Abstract
The human brain is composed of functional networks that have a modular topology, where brain regions are organized into communities that form internally dense (segregated) and externally sparse (integrated) subnetworks that underlie higher-order cognitive functioning. It is hypothesized that amyloid-β and tau pathology in preclinical Alzheimer’s disease (AD) spread through functional networks, disrupting neural communication that results in cognitive dysfunction. We used high-resolution (voxel-level) graph-based network analyses to test whether in vivo amyloid-β and tau burden was associated with the segregation and integration of brain functional connections, and episodic memory, in cognitively unimpaired Presenilin-1 E280A carriers who are expected to develop early-onset AD dementia in ∼13 y on average. Compared to noncarriers, mutation carriers exhibited less functional segregation and integration in posterior default-mode network (DMN) regions, particularly the precuneus, and in the retrospenial cortex, which has been shown to link medial temporal regions and cortical regions of the DMN. Mutation carriers also showed greater functional segregation and integration in regions connected to the salience network, including the striatum and thalamus. Greater tau burden was associated with lower segregated and integrated functional connectivity of DMN regions, particularly the precuneus and medial prefrontal cortex. In turn, greater tau pathology was related to higher segregated and integrated functional connectivity in the retrospenial cortex and the anterior cingulate cortex, a hub of the salience network. These findings enlighten our understanding of how AD-related pathology distinctly alters the brain’s functional architecture in the preclinical stage, possibly contributing to pathology propagation and ultimately resulting in dementia.
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