Whole brain segmentation of fine-grained structures using deep learning (DL) is a very challenging task since the number of anatomical labels is very high compared to the number of available training images. To address this problem, previous DL methods proposed to use a single convolution neural network (CNN) or few independent CNNs. In this paper, we present a novel ensemble method based on a large number of CNNs processing different overlapping brain areas. Inspired by parliamentary decision-making systems, we propose a framework called AssemblyNet, made of two "assemblies" of U-Nets. Such a parliamentary system is capable of dealing with complex decisions, unseen problem and reaching a relevant consensus. AssemblyNet introduces sharing of knowledge among neighboring U-Nets, an "amendment" procedure made by the second assembly at higher-resolution to refine the decision taken by the first one, and a final decision obtained by majority voting. During our validation, AssemblyNet showed competitive performance compared to state-of-the-art methods such as U-Net, Joint label fusion and SLANT. Moreover, we investigated the scan-rescan consistency and the robustness to disease effects of our method. These experiences demonstrated the reliability of AssemblyNet. Finally, we showed the interest of using semi-supervised learning to improve the performance of our method.

The chronological progression of brain atrophy over decades, from pre-symptomatic to dementia stages, has never been formally depicted in Alzheimer’s disease. This is mainly due to the lack of cohorts with long enough MRI follow-ups in cognitively unimpaired young participants at baseline. To describe a spatiotemporal atrophy staging of Alzheimer’s disease at the whole-brain level, we built extrapolated lifetime volumetric models of healthy and Alzheimer’s disease brain structures by combining multiple large-scale databases (n = 3512 quality controlled MRI from 9 cohorts of subjects covering the entire lifespan, including 415 MRI from ADNI1, ADNI2 and AIBL for Alzheimer’s disease patients). Then, we validated dynamic models based on cross-sectional data using external longitudinal data. Finally, we assessed the sequential divergence between normal aging and Alzheimer’s disease volumetric trajectories and described the following staging of brain atrophy progression in Alzheimer’s disease: (i) hippocampus and amygdala; (ii) middle temporal gyrus; (iii) entorhinal cortex, parahippocampal cortex and other temporal areas; (iv) striatum and thalamus and (v) middle frontal, cingular, parietal, insular cortices and pallidum. We concluded that this MRI scheme of atrophy progression in Alzheimer’s disease was close but did not entirely overlap with Braak staging of tauopathy, with a ‘reverse chronology’ between limbic and entorhinal stages. Alzheimer’s disease structural progression may be associated with local tau accumulation but may also be related to axonal degeneration in remote sites and other limbic-predominant associated proteinopathies.

Most digital libraries that provide user-friendly interfaces, enabling quick and intuitive access to their resources, are based on Document Image Analysis and Recognition (DIAR) methods. Such DIAR methods need ground-truthed document images to be evaluated/compared and, in some cases, trained. Especially with the advent of deep learning-based approaches, the required size of annotated document datasets seems to be ever-growing. Manually annotating real documents has many drawbacks, which often leads to small reliably annotated datasets. In order to circumvent those drawbacks and enable the generation of massive ground-truthed data with high variability, we present DocCreator, a multi-platform and open-source software able to create many synthetic image documents with controlled ground truth. DocCreator has been used in various experiments, showing the interest of using such synthetic images to enrich the training stage of DIAR tools.

Age is an important variable to describe the expected brain's anatomy status across the normal aging trajectory. The deviation from that normative aging trajectory may provide some insights into neurological diseases. In neuroimaging, predicted brain age is widely used to analyze different diseases. However, using only the brain age gap information (i.e., the difference between the chronological age and the estimated age) can be not enough informative for disease classification problems. In this paper, we propose to extend the notion of global brain age by estimating brain structure ages using structural magnetic resonance imaging. To this end, an ensemble of deep learning models is first used to estimate a 3D aging map (i.e., voxel‐wise age estimation). Then, a 3D segmentation mask is used to obtain the final brain structure ages. This biomarker can be used in several situations. First, it enables to accurately estimate the brain age for the purpose of anomaly detection at the population level. In this situation, our approach outperforms several state‐of‐the‐art methods. Second, brain structure ages can be used to compute the deviation from the normal aging process of each brain structure. This feature can be used in a multi‐disease classification task for an accurate differential diagnosis at the subject level. Finally, the brain structure age deviations of individuals can be visualized, providing some insights about brain abnormality and helping clinicians in real medical contexts.

INTRODUCTION: The three clinical variants of frontotemporal dementia (behavioral variant [bvFTD], semantic dementia, and progressive non‐fluent aphasia [PNFA]) are likely to develop over decades, from the preclinical stage to death.METHODS: To describe the long‐term chronological anatomical progression of FTD variants, we built lifespan brain charts of normal aging and FTD variants by combining 8022 quality‐controlled MRIs from multiple large‐scale data‐bases, including 107 bvFTD, 44 semantic dementia, and 38 PNFA.RESULTS: We report in this manuscript the anatomical MRI staging schemes of the three FTD variants by describing the sequential divergence of volumetric trajectories between normal aging and FTD variants. Subcortical atrophy precedes focal cortical atrophy in specific behavioral and/or language networks, with a “radiological” prodromal phase lasting 8–10 years (time elapsed between the first structural alteration and canonical cortical atrophy).DISCUSSION: Amygdalar and striatal atrophy can be candidate biomarkers for future preclinical/prodromal FTD variants definitions.Highlights: We describe the chronological MRI staging of the most affected structures in the three frontotemporal dementia (FTD) syndromic variants. In behavioral variant of FTD (bvFTD): bilateral amygdalar, striatal, and insular atrophy precedes fronto‐temporal atrophy. In semantic dementia: bilateral amygdalar atrophy precedes left temporal and hippocampal atrophy. In progressive non‐fluent aphasia (PNFA): left striatal, insular, and thalamic atrophy precedes opercular atrophy.