Functional network collapse in neurodegenerative disease.

Autor: Brown JA; University of California, San Francisco, Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, San Francisco, CA, USA., Lee AJ; University of California, San Francisco, Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, San Francisco, CA, USA., Fernhoff K; University of California, San Francisco, Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, San Francisco, CA, USA., Pistone T; University of California, San Francisco, Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, San Francisco, CA, USA., Pasquini L; University of California, San Francisco, Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, San Francisco, CA, USA., Wise AB; University of California, San Francisco, Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, San Francisco, CA, USA., Staffaroni AM; University of California, San Francisco, Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, San Francisco, CA, USA., Luisa Mandelli M; University of California, San Francisco, Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, San Francisco, CA, USA., Lee SE; University of California, San Francisco, Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, San Francisco, CA, USA., Boxer AL; University of California, San Francisco, Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, San Francisco, CA, USA., Rankin KP; University of California, San Francisco, Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, San Francisco, CA, USA., Rabinovici GD; University of California, San Francisco, Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, San Francisco, CA, USA., Luisa Gorno Tempini M; University of California, San Francisco, Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, San Francisco, CA, USA., Rosen HJ; University of California, San Francisco, Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, San Francisco, CA, USA., Kramer JH; University of California, San Francisco, Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, San Francisco, CA, USA., Miller BL; University of California, San Francisco, Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, San Francisco, CA, USA., Seeley WW; University of California, San Francisco, Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, San Francisco, CA, USA.
Jazyk: angličtina
Zdroj: BioRxiv : the preprint server for biology [bioRxiv] 2023 Dec 06. Date of Electronic Publication: 2023 Dec 06.
DOI: 10.1101/2023.12.01.569654
Abstrakt: Cognitive and behavioral deficits in Alzheimer's disease (AD) and frontotemporal dementia (FTD) result from brain atrophy and altered functional connectivity. However, it is unclear how atrophy relates to functional connectivity disruptions across dementia subtypes and stages. We addressed this question using structural and functional MRI from 221 patients with AD (n=82), behavioral variant FTD (n=41), corticobasal syndrome (n=27), nonfluent (n=34) and semantic (n=37) variant primary progressive aphasia, and 100 cognitively normal individuals. Using partial least squares regression, we identified three principal structure-function components. The first component showed overall atrophy correlating with primary cortical hypo-connectivity and subcortical/association cortical hyper-connectivity. Components two and three linked focal syndrome-specific atrophy to peri-lesional hypo-connectivity and distal hyper-connectivity. Structural and functional component scores predicted global and domain-specific cognitive deficits. Anatomically, functional connectivity changes reflected alterations in specific brain activity gradients. Eigenmode analysis identified temporal phase and amplitude collapse as an explanation for atrophy-driven functional connectivity changes.
Databáze: MEDLINE