bioRxiv Science⌕ Search

bioRxiv · 10.1101/413302

Brain age prediction of healthy subjects on anatomic MRI with deep learning: going beyond with an \"explainable AI\" mindset

Abstract

ObjectivesDefine a clinically usable preprocessing pipeline for MRI data\n\nPredict brain age using various machine learning and deep learning algorithms\n\nDefine Caveat against common machine learning traps\n\nData and MethodsWe used 1597 open-access T1 weighted MRI from 24 hospitals.\n\nPreprocessing consisted in applying : N4 bias field correction, registration to MNI152 space, white and grey stripe intensity normalization, skull stripping and brain tissue segmentation\n\nPrediction of brain age was done with growing complexity of data input (histograms, grey matter from segmented MRI, raw data) and models for training (linear models, non linear model such as gradient boosting over decision trees, and 2D and 3D convolutional neural networks).\n\nWork on interpretability consisted in (i) proceeding on basic data visualization like correlations maps between age and voxels value, and generating (ii) weights maps of simpler models, (iii) heatmaps from CNNs model with occlusion method.\n\nResultsProcessing time seemed feasible in a radiological workflow : 5 min for one 3D T1 MRI.\n\nWe found a significant correlation between age and gray matter volume with a correlation r = -0.74. Our best model obtained a mean absolute error of 3.60 years, with fine tuned convolution neural network (CNN) pretrained on ImageNet.\n\nWe carefully analyzed and interpreted the center effect.\n\nOur work on interpretability on simpler models permitted to observe heterogeneity of prediction depending on brain regions known for being involved in ageing (grey matter, ventricles). Occlusion method of CNN showed the importance of Insula and deep grey matter (thalami, caudate nuclei) in predictions.\n\nConclusionsPredicting the brain age using deep learning could be a standardized metric usable in daily neuroradiological reports. An explainable algorithm gives more confidence and acceptability for its use in practice. More clinical studies using this new quantitative biomarker in neurological diseases will show how to use it at its best.\n\nFOREWORDO_ST_ABSAbout OwkinC_ST_ABSOWKIN was co-founded in 2016 by Thomas Clozel, MD, a clinical research doctor and former assistant professor in clinical hematology and Gilles Wainrib, PhD, a pioneer in the field of Artificial Intelligence in biology. OWKIN passed the proof-of-concept phase and is now providing its innovative AI algorithms to several of the largest cancer centers and pharmaceutical companies in Europe and in the US. With offices in New York and Paris, we pride ourselves in building a company culture around transparency, collaboration, challenge, optimism and fun.\n\nOwkins teamOwkins team is international, multidisciplinary with incredible talent in machine learning, medicine and business. Our data scientists are among the best in the world, with several Kaggle Masters (top global 100), a DREAM Challenge top performer, and publications in ICML, NIPS and other top scientific journals.\n\nTasks repartitionIdea : Thomas Clozel, Roger Stup, Simon Jegou, Paul Herent\n\nBibliography : Paul Herent, Simon Jegou, Thomas Clozel\n\nData access : Simon Jegou, Paul Herent\n\nData cleaning : Simon Jegou, Paul Herent\n\nData analysis : Simon Jegou, Paul Herent\n\nData preprocessing : Simon Jegou, Paul Herent\n\nData analysis : Simon Jegou, Paul Herent\n\nTraining of models : Simon Jegou, Paul Herent\n\nWork on interpretability : Simon Jegou, Paul Herent\n\nWriting : Paul Herent\n\nRereading : Simon Jegou, Thomas Clozel, Julien Savatovsky, Roger Stupp, Olivier Elemento, Kim Gillier\n\nSubmission to medical congress : Paul Herent, Simon Jegou\n\nThanks to...\n\nSimon Jegou, for your mentoring in Machine Learning,\n\nThomas Clozel and Gilles Wainrib, for your welcome at Owkin, very benevolent, Roger Stupp, for your support and re-reading,\n\nJulien Savatovsky, for your support and re-reading,\n\nValentin Ame and Sylvain Toldo, for your help on the beautiful figures and the design of the related blogpost,\n\nAll the Owkin team members, for the great team work we did (and hope well do) between Paris and New York : Anna Huyghues Despointes, Anna I. Bondarenko, Pierre Courtiol, Derek T. Russell-Kraft, Cedric Whitney, Meriem Sefta, Vincent Lepage, Adrian Gonzalez, Maxime HE,Paul Jehanno, Raphael Leger, Alicia Simion, Eric Tramel, Mikhail Zaslavskiy, Pierre Manceron, Chloe Simpson, Paul Mabillot, Valentin Ame, Mathieu Galtier, Camille Marini, Sylvain Toldo, Charlie Saillard, Olivier Dehaene, Olivier Moindrot,\n\nPascal Roux, for your support, your help, your advices,\n\nAxelle, for your patience and support.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Herent, P., Jegou, S., Wainrib, G., Clozel, T.. 2018-09-10. Brain age prediction of healthy subjects on anatomic MRI with deep learning: going beyond with an \"explainable AI\" mindset. https://doi.org/10.1101/413302

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Rab10 and Arhgef7 interact to promote axon extension by linking vesicle supply and exocytosis

The formation of functional neural circuits begins with the extension of a single axon by immature neurons. Axon elongation requires an expansion of the plasma membrane that depends on the polarization of vesicle trafficking and exocytosis. It is not completely understood how the increased transport of vesicles into the growing axon is linked to their subsequent insertion into the plasma membrane. An analysis of early stages of neuronal differentiation indicates that an asymmetry in neurite length precedes axon specification and the accumulation of PPVs in the nascent axon. We show that increasing the transport of vesicles in unpolarized neurons is sufficient to promote the extension of additional axons. This effect indicates that an increased supply of vesicles stimulates their subsequent insertion into the membrane to allow neurite growth. The link between vesicle transport and exocytosis is mediated by the interaction of Rab10 with Arhgef7. Rab10 stimulates Arhgef7 activity on PPVs as a GEF for Cdc42b to promote axon extension through exocyst-dependent exocytosis, suggesting that their interaction links the increased supply of PPVs to their exocytosis.

neuroscience↗

Subcellular Spatial Profiling Unveils Links Between Neuritic Plaques with Selective Tau Vulnerability in Alzheimer's Disease

Alzheimer's disease (AD) features widespread extracellular amyloid-{beta} plaques but selective intraneuronal tau accumulation in cortical layers II/III and V, while layer IV remains relatively resistant. Here, we combined subcellular spatial transcriptomics with co-registered A{beta} and pTau immunohistochemistry to determine why neurons exposed to comparable plaque-associated pathology differ in somatic pTau accumulation. Plaque-associated neuritic stress occurred similarly across layers, but layer IV neurons showed attenuated pTau accumulation and reduced somatic expression of a shared neurite-soma stress program involving DCTN1, CALM3, NORAD, and PIN1. Trajectory analysis within layers identified tau-vulnerable and resistant neuronal states implicating calcium signaling, retrograde transport, and lysosomal function. Notably, astrocytic APOE-neuronal LRP1 co-expression increased significantly along the pTau-vulnerable trajectory, and APOE {epsilon}4 was associated with stronger coupling of local plaque pathology to pTau-associated molecular programs. These findings reveal neuronal programs and neuron-glia interactions underlying selective tau vulnerability and resistance in AD, highlighting potential tau-targeting therapeutics.

neuroscience↗

Widespread oscillatory suppression in autism persists in the absence of psychotropic medication.

Purpose: Investigate the neural oscillatory activity associated with autism spectrum disorder (ASD) using electroencephalographic (EEG) recordings in children and adolescents. Compare the corresponding oscillatory power between ASD patients taking psychotropic medication with a drug-naive group. Methods: ASD diagnosis was done using DSM-IV and CARS (Childhood Autism Rating Scale). EEG recordings employed 22 scalp electrodes (10/20 system). ASD vs. neurotypical groups were matched for sex and age (5 females; average age: ~10 years old). We analyzed the resting state (eyes open) EEG power spectrum during ~2-minute recordings. The multitaper FFT method was used to estimate spectral power for the delta, theta, alpha, beta and gamma frequency bands. We pooled together data from several electrodes to compute comprehensive power spectra and assess the oscillatory behavior of macro brain regions. Results: We observed widespread (~4Hz - 20Hz) oscillatory suppression comprising the theta, alpha and beta frequency bands. The most widespread and robust ASD-associated power suppression was in the high theta and alpha bands. Delta and gamma bands showed no significant power change for any of the brain regions studied. Results from a subgroup of patients (N = 9) who never used psychotropics confirmed these findings, indicating that they are not an artifact of medication. Conclusion: Suppression in theta, alpha and beta oscillations may offer insights into the neurophysiological underpinnings of autism and could be used as an accessible and comprehensive tool in ASD diagnosis, regardless of the patients being or not on medication.

neuroscience↗