A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Brain amyloid load, subjective memory complaints, and cognitive trajectories in older individuals at risk for dementia
Tekijät: Saadmaan, Gazi; Hall, Anette; Ngandu, Tiia; Kemppainen, Nina; Mangialasche, Francesca; Wittenberg, Gayle M.; Matton, Anna; Rinne, Juha O.; Kivipelto, Miia; Solomon, Alina
Kustantaja: WILEY
Kustannuspaikka: HOBOKEN
Julkaisuvuosi: 2024
Journal: European Journal of Neurology
Tietokannassa oleva lehden nimi: EUROPEAN JOURNAL OF NEUROLOGY
Lehden akronyymi: EUR J NEUROL
Artikkelin numero: e16436
Vuosikerta: 31
Numero: 12
Sivujen määrä: 5
ISSN: 1351-5101
eISSN: 1468-1331
DOI: https://doi.org/10.1111/ene.16436
Verkko-osoite: https://doi.org/10.1111/ene.16436
Rinnakkaistallenteen osoite: https://research.utu.fi/converis/portal/detail/Publication/457631324
Background and Purpose: This study evaluated associations of brain amyloid with 2-year objective and subjective cognitive measures in a trial-ready older general population at risk for dementia.
Methods: Forty-eight participants in the Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability underwent C-11-Pittsburgh compound B (PiB) positron emission tomography (PET) scans and assessment of cognition (modified Neuropsychological Test Battery [NTB]) and subjective memory complaints (Prospective and Retrospective Memory Questionnaire).
Results: Mean age was 71.4 +/- 5.06 years, and 20 participants (42%) had positive baseline PiB-PET scans. Amyloid positivity was associated with lower NTB executive function at baseline and less favorable 2-year NTB total score and memory trajectories, but not with other objective or subjective cognitive measures. Overall, there was little cognitive decline during 2 years.
Conclusions: Amyloid accumulation may affect objective but not necessarily subjective cognition from a very early at-risk stage, although substantial decline likely requires >2 years to occur.
Ladattava julkaisu This is an electronic reprint of the original article. |  |
Julkaisussa olevat rahoitustiedot:
This work was supported by the European Research Council (grant 804371); a research collaboration between Finnish Institute for Health and Welfare, Karolinska Institute, and Janssen Pharmaceutica (research project “Prediction modelling, identification and validation of novel molecular signatures of dementia”); EU Joint Program–Neurodegenerative Disease Research EURO-FINGERS and Multi-MeMo grants; an ERA PerMed Pattern-Cog grant; a NordForsk NJ-FINGERS grant; Alzheimerfonden (Sweden); the Swedish Research Council; Region Stockholm ALF (Sweden); the Center for Innovative Medicine at the Karolinska Institute (Sweden); Stiftelsen Stockholms Sjukhem (Sweden); the Knut and Alice Wallenberg Foundation (Sweden); the Swedish Research Council for Health, Working Life, and Welfare (FORTE); the Research Council of Finland; the Juho Vainio Foundation (Finland); Kela (Finland); the Ministry of Education and Culture (Finland); the Sigrid Jusélius Foundation (Finland); and the Alzheimer's Research and Prevention Foundation (USA). Janssen Research & Development provided input in study design and data interpretation. Other funding sources had no role in the design and conduct of the study; in the collection, analysis, and interpretation of the data; or in the preparation and review of the manuscript.
