Midlife insulin resistance, APOE genotype, and change in late-life brain beta-amyloid accumulation : A 5-year follow-up [11C]PIB-PET study




Pietilä Elina, Snellman Anniina, Tuisku Jouni, Helin Semi, Viitanen Matti, Jula Antti, Rinne Juha O., Ekblad Laura L.

PublisherElsevier

2024

Neurobiology of Disease

Neurobiology of Disease

106385

190

0969-9961

1095-953X

DOIhttps://doi.org/10.1016/j.nbd.2023.106385

https://doi.org/10.1016/j.nbd.2023.106385

https://research.utu.fi/converis/portal/detail/Publication/380604818



We studied if midlife insulin resistance (IR) and APOE genotype would predict brain beta-amyloid (Aβ) accumulation and Aβ change in late-life in 5-year follow-up [11C]PIB-PET study. 43 dementia-free participants were scanned twice with [11C]PIB-PET in their late-life (mean age at follow-up 75.4 years). Participants were recruited from the Finnish Health2000 study according to their HOMA-IR values measured in midlife (mean age at midlife 55.4 years; IR+ group, HOMA-IR > 2.17; IR− group, HOMA-IR <1.25), and their APOEε4 genotype. At late-life follow-up, [11C]PIB-PET composite SUVr was significantly higher in IR+ group than IR− group (median 2.3 (interquartile range 1.7–3.3) vs. 1.7 (1.5–2.4), p = 0.03). There was no difference between IR- and IR+ groups in [11C]PIB-PET SUVr 5-year change, but the change was significantly higher in IR+/APOEε4+ group (median change 0.8 (0.60–1.0)) than in IR−/APOEε4− (0.28 (0.14–0.47), p = 0.02) and in IR+/APOEε4− group (0.24 (0.06–0.40), p = 0.046). These results suggest that APOEε4 carriers with midlife IR are at increased risk for late-life Aβ accumulation.

Last updated on 2024-26-11 at 20:01