However, it remains largely unknown how network-specific and frequency-specific variability changes along the Alzheimer's disease (AD) spectrum and relates to cognitive decline. We hypothesized that cognitive impairment was related to distinct BOLD variability alterations in two brain networks with reciprocal relationship, i.e., the AD-specific default mode network (DMN) and the salience network (SN). We examined variability of resting-state fMRI data at two characteristic slow frequency-bands of slow4 (0.027-0.073 Hz) and slow5 (0.01-0.027 Hz) in 96 AD, 98 amnestic mild cognitive impairment (aMCI), and 48 age-matched healthy controls (HC) using two commonly used pre-processing pipelines. Cognition was measured with a neuropsychological assessment battery. Using both global signal regression (GSR) and independent component analysis (ICA), results generally showed a reciprocal DMN-SN variability balance in aMCI (vs. AD and/or HC), although there were distinct frequency-specific variability patterns in association with different pre-processing approaches. Importantly, lower slow4 posterior-DMN variability correlated with poorer baseline cognition/smaller hippocampus and predicted faster cognitive decline in all patients using both GSR and ICA. Altogether, our findings suggest that reciprocal DMN-SN variability balance in aMCI might represent an early signature in neurodegeneration and cognitive decline along the AD spectrum.Alzheimer's disease (AD) is the major cause of dementia, and increasing attention has been focused on early disease detection/prevention. Therefore, studying brain changes along the AD disease continuum is important, i.e., from normal aging to the prodromal stage (amnestic mild cognitive impairment, aMCI) and finally to dementia stage. Using resting-state functional connectivity methods 1-5 that quantifies the temporal synchrony between brain regions, both AD and aMCI have been found to target large-scale networks, including reduced After ICA-based denoising, there was a main effect of group mainly in the posterior DMN including the precuneus/posterior cingulate cortex and VN (cuneus), and the SN (insula) ( Supplementary Table 1). Group comparisons replicated the GSR findings that aMCI had higher variability in the posterior DMN compared with AD (precuneus; Fig. 1B, bottom panel) and HC (angular gyrus ; Fig. 1A, bottom panel), as well as lower SN variability compared with HC (insula ; Fig. 1C, bottom panel), although the latter did not survive the cluster-level Scientific RepoRtS | (2020) 10:6457 | https://doi.Furthermore, we examined whether the variability related to global cognition decline over time, defined as the difference between baseline and year 2 (year 2 minus baseline).For all correlation analyses, we focused on the brain clusters showing group differences between aMCI and HC or between AD and HC (including clusters surviving the voxel-level threshold consistently using both GSR and ICA-based denoising) (n = 3 for slow4, and n = 6 for slow5 for both data denoising methods). Correlati...
Hippocampal atrophy and abnormal β-Amyloid (Aβ) deposition are established markers of Alzheimer's disease (AD). Nonetheless, longitudinal trajectory of Aβ-associated hippocampal subfield atrophy prior to dementia remains unclear. We hypothesized that elevated Aβ correlated with longitudinal subfield atrophy selectively in no cognitive impairment (NCI), spreading to other subfields in mild cognitive impairment (MCI). We analyzed data from two independent longitudinal cohorts of nondemented elderly, including global PET-Aβ in AD-vulnerable cortical regions and longitudinal subfield volumes quantified with a novel auto-segmentation method (FreeSurfer v.6.0). Moreover, we investigated associations of Aβ-related progressive subfield atrophy with memory decline. Across both datasets, we found a converging pattern that higher Aβ correlated with faster CA1 volume decline in NCI. This pattern spread to other hippocampal subfields in MCI group, correlating with memory decline. Our results for the first time suggest a longitudinal focal-to-widespread trajectory of Aβ-associated hippocampal subfield atrophy over disease progression in nondemented elderly.Data used in preparation of this article were obtained from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database (adni.loni.usc.edu). As such, the investigators within the ADNI contributed to the design and implementation of ADNI and/or provided data but did not participate in analysis or writing of this report. A complete listing of ADNI investigators can be found at:
Introduction The SINGER pilot randomized controlled trial aims to examine the feasibility and acceptability of the Finnish Geriatric Intervention Study (FINGER) multi‐domain lifestyle interventions compared to Singaporean adaptations. Methods Seventy elderly participants were recruited and randomized into FINGER (n = 36) or SINGER (n = 34) interventions; involving physical exercise, cognitive training, diet, and vascular risk factors management, for 6 months. Results Both intervention groups were equally feasible and acceptable with participants completing at least 80% of the interventions. Body strength improved in both groups ( P upper body = .04, P lower body = .06, P core = .05). More participants in the SINGER group attained good blood pressure control at month‐6 compared to FINGER (41% vs 19%; P = .06). Discussion This study is the first to compare the feasibility of multi‐domain interventions adapted to local culture with the FINGER interventions. The findings will be utilized for a larger study to provide evidence for the efficacy of multi‐domain lifestyle interventions in preventing cognitive decline.
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