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Erratum: Author Correction: History and progress of hypotheses and clinical trials for Alzheimer's disease.

ABSTRACT: [This corrects the article DOI: 10.1038/s41392-019-0063-8.].

SUBMITTER: Liu PP

PROVIDER: S-EPMC6799801 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Erratum: Author Correction: History and progress of hypotheses and clinical trials for Alzheimer's disease.

Liu Pei-Pei PP Xie Yi Y Meng Xiao-Yan XY Kang Jian-Sheng JS

Signal transduction and targeted therapy 20190923

[This corrects the article DOI: 10.1038/s41392-019-0063-8.]. ...[more]

PMID: 31638618

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Project description:INTRODUCTION:The Alzheimer's Disease Neuroimaging Initiative (ADNI) has continued development and standardization of methodologies for biomarkers and has provided an increased depth and breadth of data available to qualified researchers. This review summarizes the over 400 publications using ADNI data during 2014 and 2015. METHODS:We used standard searches to find publications using ADNI data. RESULTS:(1) Structural and functional changes, including subtle changes to hippocampal shape and texture, atrophy in areas outside of hippocampus, and disruption to functional networks, are detectable in presymptomatic subjects before hippocampal atrophy; (2) In subjects with abnormal ?-amyloid deposition (A?+), biomarkers become abnormal in the order predicted by the amyloid cascade hypothesis; (3) Cognitive decline is more closely linked to tau than A? deposition; (4) Cerebrovascular risk factors may interact with A? to increase white-matter (WM) abnormalities which may accelerate Alzheimer's disease (AD) progression in conjunction with tau abnormalities; (5) Different patterns of atrophy are associated with impairment of memory and executive function and may underlie psychiatric symptoms; (6) Structural, functional, and metabolic network connectivities are disrupted as AD progresses. Models of prion-like spreading of A? pathology along WM tracts predict known patterns of cortical A? deposition and declines in glucose metabolism; (7) New AD risk and protective gene loci have been identified using biologically informed approaches; (8) Cognitively normal and mild cognitive impairment (MCI) subjects are heterogeneous and include groups typified not only by "classic" AD pathology but also by normal biomarkers, accelerated decline, and suspected non-Alzheimer's pathology; (9) Selection of subjects at risk of imminent decline on the basis of one or more pathologies improves the power of clinical trials; (10) Sensitivity of cognitive outcome measures to early changes in cognition has been improved and surrogate outcome measures using longitudinal structural magnetic resonance imaging may further reduce clinical trial cost and duration; (11) Advances in machine learning techniques such as neural networks have improved diagnostic and prognostic accuracy especially in challenges involving MCI subjects; and (12) Network connectivity measures and genetic variants show promise in multimodal classification and some classifiers using single modalities are rivaling multimodal classifiers. DISCUSSION:Taken together, these studies fundamentally deepen our understanding of AD progression and its underlying genetic basis, which in turn informs and improves clinical trial design.

Dataset Information

Erratum: Author Correction: History and progress of hypotheses and clinical trials for Alzheimer's disease.

Publications

Erratum: Author Correction: History and progress of hypotheses and clinical trials for Alzheimer's disease.

Similar Datasets

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