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High Contrast PET Imaging of Subcortical and Allocortical Amyloid-β in Early Alzheimer's Disease Using [11C]AZD2184
Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet & Stockholm Health Care Services, Region Stockholm, Stockholm, Sweden.
Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet & Stockholm Health Care Services, Region Stockholm, Stockholm, Sweden; PET Science Centre, Personalized Medicine and Biosamples, R&D, AstraZeneca, Stockholm, Sweden.
Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet & Stockholm Health Care Services, Region Stockholm, Stockholm, Sweden.
Örebro University, School of Medical Sciences. Department of Clinical Science and Education, Södersjukhuset, Karolinska Institutet, Stockholm, Sweden; Department of Geriatrics, Örebro University Hospital, Örebro, Sweden; Södertälje Hospital, Södertälje, Sweden.ORCID iD: 0000-0001-6863-6679
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2024 (English)In: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 98, no 4, p. 1391-1401Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Deposits of amyloid-β (Aβ) appear early in Alzheimer's disease (AD).

OBJECTIVE: The aim of the present study was to compare the presence of cortical and subcortical Aβ in early AD using positron emission tomography (PET).

METHODS: Eight cognitively unimpaired (CU) subjects, 8 with mild cognitive impairment (MCI) and 8 with mild AD were examined with PET and [11C]AZD2184. A data driven cut-point for Aβ positivity was defined by Gaussian mixture model of isocortex binding potential (BPND) values.

RESULTS: Sixteen subjects (3 CU, 5 MCI and 8 AD) were Aβ-positive. BPND was lower in subcortical and allocortical regions compared to isocortex. Fifteen of the 16 Aβ-positive subjects displayed Aβ binding in striatum, 14 in thalamus and 10 in allocortical regions.

CONCLUSIONS: Aβ deposits appear to be widespread in early AD. It cannot be excluded that deposits appear simultaneously throughout the whole brain which has implications for improved diagnostics and disease monitoring.

Place, publisher, year, edition, pages
IOS Press, 2024. Vol. 98, no 4, p. 1391-1401
Keywords [en]
Alzheimer’s disease, amygdala, amyloid deposits, entorhinal cortex, hippocampus, positron emission tomography, striatum, thalamus
National Category
Neurology
Identifiers
URN: urn:nbn:se:oru:diva-112928DOI: 10.3233/JAD-231013ISI: 001208810800005PubMedID: 38552111OAI: oai:DiVA.org:oru-112928DiVA, id: diva2:1849955
Funder
Swedish Research Council, 2015-02398AstraZenecaHedlund foundationGun och Bertil Stohnes StiftelseThe Dementia Association - The National Association for the Rights of the DementedThe Swedish Brain Foundation, FO2018-0315Region Örebro CountyStiftelsen Gamla Tjänarinnor
Note

This work was supported by a grant from the Swedish Research Council [2015-02398] (LF); by AstraZeneca Pharmaceuticals, Södertälje, Sweden; and by the Petrus and Augusta Hedlunds Foundation, the Gun and Bertil Stohnes Foundation, the Loo and Hans Osterman Foundation, the Demensförbundet, Brain Foundation “Hjärnfonden” (grant FO2018-0315), “Särfond 31 Forskning Senil demens”, Region Örebro län, “Stiftelsen för Gamla Tjänarinnor”, and Demensfonden, Stockholm (YFL).

Available from: 2024-04-09 Created: 2024-04-09 Last updated: 2024-05-24Bibliographically approved

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