| Autor: |
Groh, Jenna Rae, Svaldi, Diana, Stage, Eddie, Sanjay, Apoorva Bharthur, Logan, Paige E., Risacher, Shannon L., Saykin, Andrew J., Apostolova, Liana G. |
| Zdroj: |
Alzheimer's & Dementia: The Journal of the Alzheimer's Association; Dec2020 Supplement S11, Vol. 16 Issue 11, p1-3, 3p |
| Abstrakt: |
Background: While tau imaging is showing promise as a prognostic biomarker in Alzheimer's disease (AD), additional work is needed to fully characterize its clinical usefulness. Using a data‐driven approach, we classified individuals based on tau deposition in Braak regions and assessed how demographic, cognitive, and imaging biomarkers behaved in relation to tau deposition in the brain. Method: We included 317 ADNI participants (126 cognitively normal, 152 mild cognitive impairment, 39 dementia) with available AV1451 PET, FDG PET, AV45 PET, and MPRAGE MRI. Imaging summary variables for PET and MRI were downloaded form ADNI (http://adni.loni.usc.edu). Average AV1451 SUVR maps (Figure 2) were created in SPM 12. We used k‐means clustering to derive a two‐group solution for each Braak stage (Figure 1A) and the 75th percentile + interquartile range of the negative group from each clustering solution to define tau‐positivity. Subjects were grouped by tau positivity in Braak regions 1&2, 3&4 and 5&6. Group 000 is negative in all six regions; group 100 is negative in all regions except Braak 1&2; group 110 is only negative in Braak regions 5&6; and lastly, group 111 is positive in all regions (see Table 2). We used ANOVA with Bonferroni correction for multiple comparisons to compare demographic and cognitive, imaging biomarker measures across the groups. Result: Tau‐positive Braak 1&2 individuals (group 100) were significantly older compared to individuals with more diffuse tau positivity. Mean cortical AV45 SUVR, prevalence of amyloid positivity, and cortical hypometabolism increased with increase in tau burden (group 000<100<110<111, Table 1 and Figure 1B). Absence of significant tau binding in group 000 did not indicate lack of amyloid deposition or hypometabolism (Figure 1B). In contrast, global tau deposition (group 111) showed higher global amyloid deposition and hypometabolism (Figure 1B). Conclusion: Greater tau deposition makes individuals more likely to exhibit cognitive deficits. Absence of tau didn't correlate with absence of cognitive impairment. [ABSTRACT FROM AUTHOR] |
| Databáze: |
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