Dynamic PET imaging in patients with unilateral carotid occlusion shows lateralized cerebral hypoperfusion, but no amyloid binding
BackgroundCarotid occlusive disease is a risk factor for cognitive decline. A possible underlying etiology is that hemodynamic impairment results in decreased cerebral perfusion, exacerbated amyloid-β accumulation (Aβ) and poorer cognitive performance.ObjectiveWe aimed to determine whether patients with unilateral internal carotid artery (ICA) occlusion have less cerebral perfusion and more Aβ in the ipsilateral than in the contralateral hemisphere, and whether perfusion and Aβ are associated with cognitive functioning.MethodsWe included 20 patients (age 67.2 ± 7.0 years, 8 females, MMSE 29 [27-29]) with unilateral ICA occlusion, which underwent neuropsychological assessment and dynamic <sup>18</sup>F-Florbetaben positron emission tomography (PET). Global and regional relative perfusion (R<sub>1</sub>) and binding potential (BP<sub>ND</sub>) were obtained from the PET-images using a simplified reference tissue model. We performed Wilcoxon signed-rank tests to examine differences between hemispheres within subjects and linear regression to investigate associations with cognitive functioning.ResultsMedian global R<sub>1</sub> was 0.911 (0.883-0.950) and global BP<sub>ND</sub> was 0.172 (0.129-0.187). R<sub>1</sub> was lower in the hemisphere ipsilateral to the ICA occlusion than in the contralateral hemisphere (0.899 [0.876-0.921] versus 0.935 [0.889-0.970]). BP<sub>ND</sub> did not differ significantly between hemispheres (ipsilateral 0.172 [0.124-0.181] versus contralateral 0.168 [0.137-0.191]). Neither cerebral perfusion nor Aβ burden were associated with cognitive functioning.ConclusionsPatients with unilateral ICA occlusion did not have more Aβ in the ipsilateral hemisphere than in the contralateral hemisphere despite ipsilateral hypoperfusion. Perfusion and Aβ were unrelated to cognitive functioning. This indicates that cognitive impairment in patients with ICA occlusion is not due to exacerbated Aβ accumulation.
Authors
- Jan Willem Dankbaar (ORCID: https://orcid.org/0000-0003-4646-9587)
- Esther E. Bron (ORCID: https://orcid.org/0000-0002-5778-9263)
- Geert Jan Biessels (ORCID: https://orcid.org/0000-0001-6862-2496)
- Wiesje M. van der Flier (ORCID: https://orcid.org/0000-0001-8766-6224)
- Sebastiaan L. Meyer Viol (ORCID: https://orcid.org/0000-0001-5559-9012)
- Naomi LP Starmans (ORCID: https://orcid.org/0000-0002-8033-7126)
- Edwin Bennink (ORCID: https://orcid.org/0000-0002-3689-8532)
- L. Jaap Kappelle (ORCID: https://orcid.org/0000-0001-8665-6630)
- Sandeep S.V. Golla (ORCID: https://orcid.org/0000-0002-0721-7160)
- Nelleke Tolboom (ORCID: https://orcid.org/0000-0002-8005-2833)
- Anna E. Leeuwis
Institutions
- Erasmus MC (NL)
- University Medical Center Utrecht (NL)
- Amsterdam Neuroscience (NL)
- Amsterdam University Medical Centers (NL)
- Vrije Universiteit Amsterdam (NL)
- Erasmus University Rotterdam (NL)
Publication Details
- Journal
- Journal of Alzheimer s Disease
- Published
- 2025-04-17
- DOI
- https://doi.org/10.1177/13872877251329593
- Primary Topic
- Cerebrovascular and Carotid Artery Diseases
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Hartstichting