APOE4 carriership status influences [11C]PiB white matter retention in cognitively healthy older adults - UTU Tutkimustietojärjestelmä

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APOE4 carriership status influences [11C]PiB white matter retention in cognitively healthy older adults

Tekijät: Tato-Fernández Claudia; Ekblad Laura L.; Bucci Marco; Tuisku Jouni; Parkkola Riitta; Helin Semi; Rinne Juha O.; Snellman Anniina

Kustantaja: Elsevier BV

Julkaisuvuosi: 2025

Lehti:: Neurobiology of Disease

Artikkelin numero: 107140

Vuosikerta: 216

ISSN: 0969-9961

eISSN: 1095-953X

DOI: https://doi.org/10.1016/j.nbd.2025.107140

Verkko-osoite: https://doi.org/10.1016/j.nbd.2025.107140

Rinnakkaistallenteen osoite: https://research.utu.fi/converis/portal/detail/Publication/504654705

Tiivistelmä

Purpose: The objective of this study was to assess whether APOE4 carriership status affects white matter (WM) [¹¹C]PiB positron emission tomography (PET) retention in cognitively healthy older adults, as a potential indicator of myelin integrity.

Methods: We explored WM [¹¹C]PiB retention of 101 participants (non-carriers, n = 40; APOE3/4 carriers, n = 40; APOE4/4 carriers, n = 21) and its association with fractional anisotropy, a diffusion tensor imaging measure reflecting WM microstructure. WM [¹¹C]PiB retention was assessed in voxel-wise analysis and within normal-appearing white matter (NAWM) and white matter hyperintensities (WMHs) as regions-of-interest.

Results: [¹¹C]PiB retention was lower in WMHs than NAWM (p_t-test < 0.001). In NAWM, APOE4/4 and APOE3/4 carriers showed reduced [¹¹C]PiB retention compared to non-carriers (p_ANCOVA = 0.040, among all groups), while there were no significant differences in [¹¹C]PiB retention within regions of WMHs (p_ANCOVA = 0.11). APOE4/4 carriers had lower WM [¹¹C]PiB retention than non-carriers in voxel-wise analysis (p_FWE < 0.05). WM [¹¹C]PiB retention was not associated with fractional anisotropy, suggesting different pathological pathways.

Conclusion: A decrease in NAWM [¹¹C]PiB retention is suggestive of myelin damage prior to the onset of cognitive decline in APOE4 homozygotes.

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Julkaisussa olevat rahoitustiedot:
CT received funding for this project from the Finnish Cultural Foundation, the Finnish Brain Foundation, Finnish Governmental Research Funding (VTR) and the University of Turku Graduate School. LLE was funded by the Finnish Medical Foundation, the Diabetes Research Foundation and by Finnish Governmental Research Funding (VTR) and she received project funding for the CIRI-5Y study from the Juho Vainio Foundation. JOR was funded by the Sigrid Juselius Foundation and Finnish Governmental Research Funding (VTR). AS was funded by the Research Council of Finland (grant number 341059), the Emil Aaltonen Foundation, the Paulo Foundation, Finnish Governmental Research Funding (VTR) and the Orion Research Foundation sr directly related to this study.