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Cerebral atrophy in mild cognitive impairment and Alzheimer disease: rates and acceleration.
Full text linkOBJECTIVE: To quantify the regional and global cerebral atrophy rates and assess acceleration rates in healthy controls, subjects with mild cognitive impairment (MCI), and subjects with mild Alzheimer disease (AD). METHODS: Using 0-, 6-, 12-, 18-, 24-, and 36-month MRI scans of controls and subjects with MCI and AD from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database, we calculated volume change of whole brain, hippocampus, and ventricles between all pairs of scans using the boundary shift integral. RESULTS: We found no evidence of acceleration in whole-brain atrophy rates in any group. There was evidence that hippocampal atrophy rates in MCI subjects accelerate by 0.22%/year2 on average (p = 0.037). There was evidence of acceleration in rates of ventricular enlargement in subjects with MCI (p = 0.001) and AD (p < 0.001), with rates estimated to increase by 0.27 mL/year2 (95% confidence interval 0.12, 0.43) and 0.88 mL/year2 (95% confidence interval 0.47, 1.29), respectively. A post hoc analysis suggested that the acceleration of hippocampal loss in MCI subjects was mainly driven by the MCI subjects that were observed to progress to clinical AD within 3 years of baseline, with this group showing hippocampal atrophy rate acceleration of 0.50%/year2 (p = 0.003). CONCLUSIONS: The small acceleration rates suggest a long period of transition to the pathologic losses seen in clinical AD. The acceleration in hippocampal atrophy rates in MCI subjects in the ADNI seems to be driven by those MCI subjects who concurrently progressed to a clinical diagnosis of AD
OAI services in Academicians: Looking Forward
No full textThe main focus of this paper is to look the forward of Open Access Initiative (OAI) in academicians Were to be tried and perhaps implemented on a global academicians it must made known to the local audience first. This can only be achieved if the OAI services in academicians services such as ‘Information Society’. In the case of the OAI services in academicians used in the study; it has benefits directly or indirectly and eventually become more accepted
adni-netwas: v1.0
No full text<p>This is the version of our analysis code associated with the analyses described in the submission of Song et al. to BioData Mining.</p>
A voxel‐based morphometry comparison of the 3.0T ADNI‐1 and ADNI‐2 volumetric MRI protocols
Full text linkObjectivesThe Alzheimer's Disease Neuroimaging Initiative 3.0T MRI image acquisition scheme changed between the original ADNI-1 grant and the two subsequent grants (ADNI-GO and ADNI-2). The aim of the current study was to investigate the compatibility of the 3.0T ADNI-1 and ADNI-2 T1-weighted volumes using voxel-based morphometry (VBM).MethodsT1-weighted images of 30 subjects were acquired using a 3T GE Signa HDx using the ADNI-1 and ADNI-2 T1-weighted volume sequences. Images were pre-processed and analysed using SPM8. Global grey matter (GM), white matter (WM) and cerebrospinal fluid (CSF) volumes were compared, as well as voxel-by-voxel differences in GM and WM.ResultsCorrelation coefficients and percentage differences for each tissue type between ADNI-1 and ADNI-2 were as follows: ((GM: intraclass correlation coefficient (ICC) = 0.86, ADNI-1 3.09% < ADNI-2) (WM: ICC = 0.91, ADNI-1 2.92% > ADNI-2) (CSF: ICC = 0.90, ADNI-1 1.94% > ADNI-2)). For ADNI-2, widespread increases in GM were found relative to ADNI-1 (cerebellum and pre-central gyrus), with localised decreases along the midline and temporal lobes. For ADNI-1, widespread increases in WM were found relative to ADNI-2 (cerebellum and pre-central gyrus), together with localised decreases in the temporal gyrus.ConclusionsThe widespread increase in GM and localised decrease in WM in ADNI-2 compared to ADNI-1 images suggests that the image acquisition protocols are not directly comparable using SPM-8. Total volumes of GM, WM and CSF also differed between the protocols in the following order of magnitude: GM > WM > CSF. This has implications for studies aiming to analyse images acquired using the ADNI-1 and ADNI-2 protocols under VBM
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Overview of ADNI MRI
Full text linkThe magnetic resonance imaging (MRI) Core has been operating since Alzheimer's Disease Neuroimaging Initiative's (ADNI) inception, providing 20 years of data including reliable, multi-platform standardized protocols, carefully curated image data, and quantitative measures provided by expert investigators. The overarching purposes of the MRI Core include: (1) optimizing and standardizing MRI acquisition methods, which have been adopted by many multicenter studies and trials worldwide and (2) providing curated images and numeric summary values from relevant MRI sequences/contrasts to the scientific community. Over time, ADNI MRI has become increasingly complex. To remain technically current, the ADNI MRI protocol has changed substantially over the past two decades. The ADNI 4 protocol contains nine different imaging types (e.g., three dimensional [3D] T1-weighted and fluid-attenuated inversion recovery [FLAIR]). Our view is that the ADNI MRI data are a greatly underutilized resource. The purpose of this paper is to educate the scientific community on ADNI MRI methods and content to promote greater awareness, accessibility, and use. HIGHLIGHTS: The MRI Core provides multi-platform standardized protocols, carefully curated image data, and quantitative analysis by expert groups. The ADNI MRI protocol has undergone major changes over the past two decades to remain technically current. As of April 25, 2024, the following numbers of image series are available: 17,141 3D T1w; 6877 FLAIR; 3140 T2/PD; 6623 GRE; 3237 dMRI; 2846 ASL; 2968 TF-fMRI; and 2861 HighResHippo (see Table 1 for abbreviations). As of April 25, 2024, the following numbers of quantitative analyses are available: FreeSurfer 10,997; BSI 6120; tensor based morphometry (TBM) and TBM-SYN 12,019; WMH 9944; dMRI 1913; ASL 925; TF-fMRI NFQ 2992; and medial temporal subregion volumes 2726 (see Table 4 for abbreviations). ADNI MRI is an underutilized resource that could be more useful to the research community
Lack of association between bridging integrator 1 ( BIN1 ) rs744373 polymorphism and tau\u2010PET load in cognitively intact older adults
No full textAbstract: Introduction: The bridging integrator 1(BIN1) rs744373 risk polymorphism has been linked to increased [18F]AV1451 signal in non-demented older adults (ie., mild cognitive impairment [MCI] plus cognitively normal [CN] individuals). However, the association of BIN1 with in vivo tau, amyloid beta (A\u3b2) burden, and cognitive impairment in the asymptomatic stage of Alzheimer's disease (AD) remains unknown. Methods: The BIN1 effect on [18F]AV1451 binding was evaluated in 59 cognitively normal (CN) participants (39% apolipoprotein E [APOE \u3b54]) from the Flemish Prevent AD Cohort KU Leuven (F-PACK), as well as in 66 Alzheimer's Disease Neuroimaging Initiative (ADNI) CN participants, using voxelwise and regional statistics. For comparison, 52 MCI patients from ADNI were also studied. Results: Forty-four percent of F-PACK participants were BIN1 rs744373 risk-allele carriers, 21% showed high amyloid burden, and 8% had elevated [18F]AV1451 binding. In ADNI, 53% and 50% of CNs and MCIs, respectively, carried the BIN1 rs744373 risk-allele. Amyloid positivity was present in 23% of CNs and 51% of MCIs, whereas 2% of CNs and 35% of MCIs showed elevated [18F]AV1451 binding. There was no significant effect of BIN1 on voxelwise or regional [18F]AV1451 in F-PACK or ADNI CNs, or in the pooled CN sample. No significant association between BIN1 and [18F]AV1451 was obtained in ADNI MCI patients. However, in the MCI group, numerically higher [18F]AV1451 binding was observed in the BIN1 risk-allele group compared to the BIN1 normal group in regions corresponding to more progressed tau pathology. Discussion: We could not confirm the association between BIN1 rs744373 risk-allele and elevated [18F]AV1451 signal in CN older adults or MCI. Numerically higher [18F]AV1451 binding was observed, however, in the MCI BIN1 risk-allele group, indicating that the previously reported positive effect may be confounded by group. Therefore, when studying how the BIN1 risk polymorphism influences AD pathogenesis, a distinction should be made between asymptomatic, MCI, and dementia stages of AD
Influence of APOE Genotype on Hippocampal Atrophy over Time - An N=1925 Surface-Based ADNI Study
Full text linkabstract: The apolipoprotein E (APOE) e4 genotype is a powerful risk factor for late-onset Alzheimer’s disease (AD). In the Alzheimer’s Disease Neuroimaging Initiative (ADNI) cohort, we previously reported significant baseline structural differences in APOE e4 carriers relative to non-carriers, involving the left hippocampus more than the right—a difference more pronounced in e4 homozygotes than heterozygotes. We now examine the longitudinal effects of APOE genotype on hippocampal morphometry at 6-, 12- and 24-months, in the ADNI cohort. We employed a new automated surface registration system based on conformal geometry and tensor-based morphometry. Among different hippocampal surfaces, we computed high-order correspondences, using a novel inverse-consistent surface-based fluid registration method and multivariate statistics consisting of multivariate tensor-based morphometry (mTBM) and radial distance. At each time point, using Hotelling’s T[superscript 2] test, we found significant morphological deformation in APOE e4 carriers relative to non-carriers in the full cohort as well as in the non-demented (pooled MCI and control) subjects at each follow-up interval. In the complete ADNI cohort, we found greater atrophy of the left hippocampus than the right, and this asymmetry was more pronounced in e4 homozygotes than heterozygotes. These findings, combined with our earlier investigations, demonstrate an e4 dose effect on accelerated hippocampal atrophy, and support the enrichment of prevention trial cohorts with e4 carriers.The article is published at http://journals.plos.org/plosone/article?id=10.1371/journal.pone.015290
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