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The amyloid hypothesis posits that accumulation of amyloid is primarily responsible for the accumulation of tau tangles, synaptic dysfunction, neurodegeneration, and cognitive decline especially in memory function, which characterizes Alzheimer's disease (AD) as an amyloid facilitated tauopathy. We investigated whether local tau deposition is associated with local amyloid burden (LAB) and the retrospective annualized amyloid accumulation rate (RA3R) in early symptomatic stages of AD.


Flops Plain Red Beet Sandals Shoes Bridal or Ivory Satin Bridesmaid straps White Flip wrapped Wedges Wedding 21 older adults (1 cognitively normal, 5 with early mild cognitive impairment (MCI), 8 with subjective memory complaint and 7 with late-MCI; 77.6 ± 6.3 y) received longitudinal AV45-PET and structural-MRI scans (1.99 ± 0.03 y follow-up duration) and cross-sectional AV1451-PET for tau deposition at the end of the study. AV1451-SUVR and AV45-SUVR maps were co-registered to corresponding structural-MRIs, all nonlinearly warped to the MNI template. Local RA3Rs were calculated from longitudinal AV45-SUVR maps. Using voxel-wise linear regression models (LRM) with age, gender, education, ApoE4-status, and CDR at AV1451-PET scan time as covariates, we characterized 1) LAB and tau deposition associations cross-sectionally and 2) local associations between RA3R and tau deposition. Furthermore, we examined non-local RA3R and tau deposition associations across different brain regions using parallel independent component analysis (ICA).


Voxel-wise LRM revealed positive association between LAB and tau deposition cross-sectionally, predominantly in the medial temporal and lateral occipital cortices (Figure 1-A; p<0.05 FDR corrected). Voxel-wise RA3R and tau deposition associations were localized to left lateral frontal cortices (Figure 1-B; p<0.05 FDR corrected). Parallel-ICA analysis revealed covarying (r=0.36; p=0.0006) patterns of increased rates of amyloid accumulation (retrospective) predominantly in the right temporal lobe retrospectively and increased tau deposition bilaterally in the medial temporal cortices and left lateral temporal and frontal cortices (Figure 2; z>2.5).


Tau deposition in early symptomatic stages of AD shows significant positive associations with both LAB and RA3R. Non-local associations, in particular, linking increased amyloid accumulation rates in frontal and lateral temporal cortices with increased tau deposition in medial temporal cortices, are of great interest and supports the idea that the disease pathology spread follows the brain’s intrinsic connectivity networks and potential remote effects of amyloid via the brain networks.

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