Increased Cortical Thickness in Alzheimer's Disease.


Journal

Annals of neurology
ISSN: 1531-8249
Titre abrégé: Ann Neurol
Pays: United States
ID NLM: 7707449

Informations de publication

Date de publication:
24 Feb 2024
Historique:
revised: 31 01 2024
received: 16 06 2023
accepted: 03 02 2024
medline: 24 2 2024
pubmed: 24 2 2024
entrez: 24 2 2024
Statut: aheadofprint

Résumé

Patients with Alzheimer's disease (AD) have diffuse brain atrophy, but some regions, such as the anterior cingulate cortex (ACC), are spared and may even show increase in size compared to controls. The extent, clinical significance, and mechanisms associated with increased cortical thickness in AD remain unknown. Recent work suggested neural facilitation of regions anticorrelated to atrophied regions in frontotemporal dementia. Here, we aim to determine whether increased thickness occurs in sporadic AD, whether it relates to clinical symptoms, and whether it occur in brain regions functionally connected to-but anticorrelated with-locations of atrophy. Cross-sectional clinical, neuropsychological, and neuroimaging data from the Alzheimer's Disease Neuroimaging Initiative were analyzed to investigate cortical thickness in AD subjects versus controls. Atrophy network mapping was used to identify brain regions functionally connected to locations of increased thickness and atrophy. AD patients showed increased thickness in the ACC in a region-of-interest analysis and the visual cortex in an exploratory analysis. Increased thickness in the left ACC was associated with preserved cognitive function, while increased thickness in the left visual cortex was associated with hallucinations. Finally, we found that locations of increased thickness were functionally connected to, but anticorrelated with, locations of brain atrophy (r = -0.81, p < 0.05). Our results suggest that increased cortical thickness in Alzheimer's disease is relevant to AD symptoms and preferentially occur in brain regions functionally connected to, but anticorrelated with, areas of brain atrophy. Implications for models of compensatory neuroplasticity in response to neurodegeneration are discussed. ANN NEUROL 2024.

Identifiants

pubmed: 38400760
doi: 10.1002/ana.26894
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : NIH HHS
ID : 1K23AG070320-01A1
Pays : United States
Organisme : NIH HHS
ID : R56AG069086
Pays : United States
Organisme : Alzheimer's Association
Pays : United States

Informations de copyright

© 2024 The Authors. Annals of Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.

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Auteurs

Tony X Phan (TX)

Department of Neurology, Vanderbilt University Medical Center, Nashville, TN.

Sheena Baratono (S)

Center for Brain Circuit Therapeutics, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.

William Drew (W)

Center for Brain Circuit Therapeutics, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.

Aaron M Tetreault (AM)

Department of Neurology, Vanderbilt University Medical Center, Nashville, TN.

Michael D Fox (MD)

Center for Brain Circuit Therapeutics, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.

R Ryan Darby (RR)

Department of Neurology, Vanderbilt University Medical Center, Nashville, TN.

Classifications MeSH