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Change in brain amyloid load and cognition in patients with amnestic mild cognitive impairment: a 3-year follow-up study

BACKGROUND: Our aim was to investigate the discriminative value of (18)F-Flutemetamol PET in longitudinal assessment of amyloid beta accumulation in amnestic mild cognitive impairment (aMCI) patients, in relation to longitudinal cognitive changes. METHODS: We investigated the change in (18)F-Fluteme...

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Detalles Bibliográficos
Autores principales: Rauhala, Elina, Johansson, Jarkko, Karrasch, Mira, Eskola, Olli, Tolvanen, Tuula, Parkkola, Riitta, Virtanen, Kirsi A., Rinne, Juha O.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9445147/
https://www.ncbi.nlm.nih.gov/pubmed/36065070
http://dx.doi.org/10.1186/s13550-022-00928-5
Descripción
Sumario:BACKGROUND: Our aim was to investigate the discriminative value of (18)F-Flutemetamol PET in longitudinal assessment of amyloid beta accumulation in amnestic mild cognitive impairment (aMCI) patients, in relation to longitudinal cognitive changes. METHODS: We investigated the change in (18)F-Flutemetamol uptake and cognitive impairment in aMCI patients over time up to 3 years which enabled us to investigate possible association between changes in brain amyloid load and cognition over time. Thirty-four patients with aMCI (mean age 73.4 years, SD 6.6) were examined with (18)F-Flutemetamol PET scan, brain MRI and cognitive tests at baseline and after 3-year follow-up or earlier if the patient had converted to Alzheimer´s disease (AD). (18)F-Flutemetamol data were analyzed both with automated region-of-interest analysis and voxel-based statistical parametric mapping. RESULTS: (18)F-flutemetamol uptake increased during the follow-up, and the increase was significantly higher in patients who were amyloid positive at baseline as compared to the amyloid-negative ones. At follow-up, there was a significant association between (18)F-Flutemetamol uptake and MMSE, logical memory I (immediate recall), logical memory II (delayed recall) and verbal fluency. An association was seen between the increase in (18)F-Flutemetamol uptake and decline in MMSE and logical memory I scores. CONCLUSIONS: In the early phase of aMCI, presence of amyloid pathology at baseline strongly predicted amyloid accumulation during follow-up, which was further paralleled by cognitive declines. Inversely, some of our patients remained amyloid negative also at the end of the study without significant change in (18)F-Flutemetamol uptake or cognition. Future studies with longer follow-up are needed to distinguish whether the underlying pathophysiology of aMCI in such patients is other than AD.