Autor: |
Seyed Hani Hojjati, Tracy A. Butler, Gloria C. Chiang, Christian Habeck, Arindam RoyChoudhury, Farnia Feiz, Jacob Shteingart, Siddharth Nayak, Sindy Ozoria, Antonio Fernández, Yaakov Stern, José A. Luchsinger, Davangere P. Devanand, Qolamreza R. Razlighi |
Jazyk: |
angličtina |
Rok vydání: |
2023 |
Předmět: |
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Zdroj: |
NeuroImage: Clinical, Vol 38, Iss , Pp 103409- (2023) |
Druh dokumentu: |
article |
ISSN: |
2213-1582 |
DOI: |
10.1016/j.nicl.2023.103409 |
Popis: |
Alzheimer's disease (AD) is defined by the presence of Amyloid-β (Aβ), tau, and neurodegeneration (ATN framework) in the human cerebral cortex. Yet, prior studies have suggested that Aβ deposition can be associated with both cortical thinning and thickening. These contradictory results are attributed to small sample sizes, the presence versus absence of tau, and limited detectability in the earliest phase of protein deposition, which may begin in young adulthood and cannot be captured in studies enrolling only older subjects. In this study, we aimed to find the distinct and joint effects of Aβ and tau on neurodegeneration during the progression from normal to abnormal stages of pathologies that remain elusive. We used 18F-MK6240 and 18F-Florbetaben/18F-Florbetapir positron emission tomography (PET) and magnetic resonance imaging (MRI) to quantify tau, Aβ, and cortical thickness in 590 participants ranging in age from 20 to 90. We performed multiple regression analyses to assess the distinct and joint effects of Aβ and tau on cortical thickness using 590 healthy control (HC) and mild cognitive impairment (MCI) participants (141 young, 394 HC elderlies, 52 MCI). We showed that in participants with normal levels of global Aβ deposition, Aβ uptake was significantly associated with increased cortical thickness regardless of tau (e.g., left entorhinal cortex with t > 3.241, p |
Databáze: |
Directory of Open Access Journals |
Externí odkaz: |
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