Lobar Microbleeds in the Posterior Cortical Atrophy Syndrome: A Comparison to Typical Alzheimer's Disease.

Alzheimer’s disease Atypical Alzheimer’s disease Cerebral amyloid angiopathy Lobar microbleeds Posterior cortical atrophy

Journal

Current neurology and neuroscience reports
ISSN: 1534-6293
Titre abrégé: Curr Neurol Neurosci Rep
Pays: United States
ID NLM: 100931790

Informations de publication

Date de publication:
23 Jan 2024
Historique:
accepted: 14 12 2023
medline: 23 1 2024
pubmed: 23 1 2024
entrez: 23 1 2024
Statut: aheadofprint

Résumé

Posterior cortical atrophy is a clinico-radiographical syndrome that presents with higher-order visual dysfunction and is most commonly due to Alzheimer's disease. Understanding factors associated with atypical presentations of Alzheimer's disease, such as posterior cortical atrophy (PCA), holds promise to shape our understanding of AD pathophysiology. Thus, we aimed to compare MRI evidence of lobar microbleeds (LMBs) in posterior cortical atrophy (PCA) syndrome to typical AD (tAD) and to assess and compare MRI evidence of cerebral amyloid angiopathy (CAA) in each group. We retrospectively collected clinical and MRI data from participants with PCA (n = 26), identified from an institutional PCA registry, and participants with tAD (n = 46) identified from electronic health records from a single institution. LMBs were identified on susceptibility-weighted imaging (SWI); the Fazekas grade of white matter disease was assessed using FLAIR images, and Boston criteria version 2.0 for cerebral amyloid angiopathy were applied to all data. The proportion of participants with PCA and LMB (7.7%) was lower than for tAD (47.8%) (p = 0.005). The frequency of "probable" CAA was similar in both groups, while "possible" CAA was more frequent in tAD (30.4%) than PCA (0%) (p = 0.001). The Fazekas grades were not different between groups. Lobar microbleeds on SWI were not more common in PCA than in typical AD. Clinicopathological investigations are necessary to confirm these findings. The factors that contribute to the posterior cortical atrophy phenotype are unknown.

Identifiants

pubmed: 38261145
doi: 10.1007/s11910-024-01330-5
pii: 10.1007/s11910-024-01330-5
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

Auteurs

Victoria S Pelak (VS)

Department of Neurology, University of Colorado School of Medicine, 12631 East 17 Avenue, Mail Stop B185, Aurora, CO, 80045, USA. Victoria.Pelak@CUAnschutz.edu.

Vishal Krishnan (V)

Department of Neurology, University of Colorado School of Medicine, 12631 East 17 Avenue, Mail Stop B185, Aurora, CO, 80045, USA.

Stephanie Serva (S)

Department of Neurology, University of Colorado School of Medicine, 12631 East 17 Avenue, Mail Stop B185, Aurora, CO, 80045, USA.

Peter Pressman (P)

Department of Neurology, University of Colorado School of Medicine, 12631 East 17 Avenue, Mail Stop B185, Aurora, CO, 80045, USA.

Asher Mahmood (A)

Department of Neurology, University of Colorado School of Medicine, 12631 East 17 Avenue, Mail Stop B185, Aurora, CO, 80045, USA.

Lily Noteboom (L)

Department of Neurology, University of Colorado School of Medicine, 12631 East 17 Avenue, Mail Stop B185, Aurora, CO, 80045, USA.

Brianne M Bettcher (BM)

Department of Neurology, University of Colorado School of Medicine, 12631 East 17 Avenue, Mail Stop B185, Aurora, CO, 80045, USA.

Stefan H Sillau (SH)

Department of Neurology, University of Colorado School of Medicine, 12631 East 17 Avenue, Mail Stop B185, Aurora, CO, 80045, USA.

Andrew L Callen (AL)

Department of Radiology, University of Colorado School of Medicine, Aurora, CO, USA.

Ashesh A Thaker (AA)

Department of Radiology, University of Colorado School of Medicine, Aurora, CO, USA.

Classifications MeSH