Tackling energy poverty through social intrapreneurship in large-scale energy companies

Purpose: The purpose of this paper is to present advances towards a social intrapreneurship department within energy corporations. By drawing on the literature on social intrapreneurship and stakeholder theory, this paper provides a conceptual proposal for an organisational structure. This paper builds on the notion of bridging and boundary organisations, to suggest an organisational innovative structure as a social intrapreneurship endeavour focussing on the increasing salience of weak stakeholders in energy corporations from the energy justice approach. Design/methodology/approach: This paper draws on the literatures on social intrapreneurship and stakeholder theory, to provide arguments and an organisational proposal to alleviate energy poverty in energy corporations. Findings: The results are presented in a conceptual process model for the development of Social Energy Department units within large energy companies, illustrating their embeddedness in both societal and company-level processes to facilitate social intrapreneurship initiatives that would alleviate energy poverty in the just transition. Practical implications: The paper promises novel insights at the nexus of social enterprise and organisational change. The practical applicability is particularly promising, as it focusses on integrating novel units in energy companies and stimulates further research on models of social intrapreneurship to tackle energy poverty. Originality/value: The paper offers both practical and theoretical contributions to the stakeholder theory field with insights from social intrapreneurship and organisational stakeholder theory in the context of a specific social problem – energy poverty, energy justice and the just energy transition

Brain Communications

Brain charts for the human lifespan have been recently proposed to build dynamic models of brain anatomy in normal aging and various neurological conditions. They offer new possibilities to quantify neuroanatomical changes from preclinical stages to death, where longitudinal MRI data are not available. In this study, we used brain charts to model the progression of brain atrophy in progressive supranuclear palsy – Richardson syndrome (PSPRS). We combined multiple datasets (n=8170 quality controlled MRI of healthy subjects from 22 cohorts covering the entire lifespan, and n=62 MRI of PSP-RS patients from the 4 Repeat Tauopathy Neuroimaging Initiative) to extrapolate lifetime volumetric models of healthy and PSP-RS brain structures. We then mapped in time and space the sequential divergence between healthy and PSP-RS charts. We found six major consecutive stages of atrophy progression: (i) ventral diencephalon (including subthalamic nuclei, substantia nigra, and red nuclei), (ii) pallidum, (iii) brainstem, striatum and amygdala, (iv) thalamus, (v) frontal lobe and (vi) occipital lobe. The three structures with most severe atrophy over time were the thalamus, followed by the pallidum and the brainstem. These results match the neuropathological staging of tauopathy progression in PSP-RS, where the pathology is supposed to start in the pallido-nigro-luysian system and spreads rostrally via the striatum and the amygdala to the cerebral cortex, and caudally to the brainstem. This study supports the use of brain charts for the human lifespan to study the progression of neurodegenerative diseases, especially in the absence of specific biomarkers as in PSP.Apprentissage profond pour la volumétrie cérébrale : vers le BigData en neuroscienceInitiative d'excellence de l'Université de Bordeau

Brain Commun.

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. © 2022 The Author(s). Published by Oxford University Press on behalf of the Guarantors of Brain.Apprentissage profond pour la volumétrie cérébrale : vers le BigData en neuroscienceTranslational Research and Advanced Imaging Laborator

Long-term antipsychotic and benzodiazepine use. and brain volume changes in schizophrenia : The Northern Finland Birth Cohort 1966 study

High doses of antipsychotics have been associated with loss in cortical and total gray matter in schizophrenia. However, previous imaging studies have not taken benzodiazepine use into account, in spite of evidence suggesting adverse effects such as cognitive impairment and increased mortality. In this Northern Finland Birth Cohort 1966 study, 69 controls and 38 individuals with schizophrenia underwent brain MRI at the ages of 34 and 43 years. At baseline, the average illness duration was over 10 years. Brain structures were delineated using an automated volumetry system, volBrain, and medication data on cumulative antipsychotic and benzodiazepine doses were collected using medical records and interviews. We used linear regression with intracranial volume and sex as covariates; illness severity was also taken into account. Though both medication doses associated to volumetric changes in subcortical structures, after adjusting for each other and the average PANSS total score, higher scan-interval antipsychotic dose associated only to volume increase in lateral ventricles and higher benzodiazepine dose associated with volume decrease in the caudate nucleus. To our knowledge, there are no previous studies reporting associations between benzodiazepine dose and brain structural changes. Further studies should focus on how these observations correspond to cognition and functioning.Peer reviewe

Comparing fully automated state-of-the-art cerebellum parcellation from magnetic resonance images

[EN] The human cerebellum plays an essential role in motor control, is involved in cognitive function (i.e., attention, working memory, and language), and helps to regulate emotional responses. Quantitative in-vivo assessment of the cerebellum is important in the study of several neurological diseases including cerebellar ataxia, autism, and schizophrenia. Different structural subdivisions of the cerebellum have been shown to correlate with differing pathologies. To further understand these pathologies, it is helpful to automatically parcellate the cerebellum at the highest fidelity possible. In this paper, we coordinated with colleagues around the world to evaluate automated cerebellum parcellation algorithms on two clinical cohorts showing that the cerebellum can be parcellated to a high accuracy by newer methods. We characterize these various methods at four hierarchical levels: coarse (i.e., whole cerebellum and gross structures), lobe, subdivisions of the vermis, and the lobules. Due to the number of labels, the hierarchy of labels, the number of algorithms, and the two cohorts, we have restricted our analyses to the Dice measure of overlap. Under these conditions, machine learning based methods provide a collection of strategies that are efficient and deliver parcellations of a high standard across both cohorts, surpassing previous work in the area. In conjunction with the rank-sum computation, we identified an overall winning method.The data collection and labeling of the cerebellum was supported in part by the NIH/NINDS grant R01 NS056307 (PI: J.L. Prince) and NIH/NIMH grants R01 MH078160 & R01 MH085328 (PI: S.H. Mostofsky). PMT is supported in part by the NIH/NIBIB grant U54 EB020403. CERES2 development was supported by grant UPV2016-0099 from the Universitat Politecnica de Valencia (PI: J.V. Manjon); the French National Research Agency through the Investments for the future Program IdEx Bordeaux (ANR-10-IDEX-03-02, HL-MRI Project; PI: P. Coupe) and Cluster of excellence CPU and TRAIL (HR-DTI ANR-10-LABX-57; PI: P. Coupe). Support for the development of LiviaNET was provided by the National Science and Engineering Research Council of Canada (NSERC), discovery grant program, and by the ETS Research Chair on Artificial Intelligence in Medical Imaging. The authors wish to acknowledge the invaluable contributions offered by Dr. George Fein (Dept. of Medicine and Psychology, University of Hawaii) in preparing this manuscript.Carass, A.; Cuzzocreo, JL.; Han, S.; Hernandez-Castillo, CR.; Rasser, PE.; Ganz, M.; Beliveau, V.... (2018). Comparing fully automated state-of-the-art cerebellum parcellation from magnetic resonance images. NeuroImage. 183:150-172. https://doi.org/10.1016/j.neuroimage.2018.08.003S15017218

Heterozygous and Homozygous Variants in SORL1 Gene in Alzheimer's Disease Patients: Clinical, Neuroimaging and Neuropathological Findings

In the last few years, the SORL1 gene has been strongly implicated in the development of Alzheimer’s disease (AD). We performed whole-exome sequencing on 37 patients with early-onset dementia or family history suggestive of autosomal dominant dementia. Data analysis was based on a custom panel that included 46 genes related to AD and dementia. SORL1 variants were present in a high proportion of patients with candidate variants (15%, 3/20). We expand the clinical manifestations associated with the SORL1 gene by reporting detailed clinical and neuroimaging findings of six unrelated patients with AD and SORL1 mutations. We also present for the first time a patient with the homozygous truncating variant c.364C>T (p.R122*) in SORL1, who also had severe cerebral amyloid angiopathy. Furthermore, we report neuropathological findings and immunochemistry assays from one patient with the splicing variant c.4519+5G>A in the SORL1 gene, in which AD was confirmed by neuropathological examination. Our results highlight the heterogeneity of clinical presentation and familial dementia background of SORL1-associated AD and suggest that SORL1 might be contributing to AD development as a risk factor gene rather than as a major autosomal dominant gene.This work was supported by the Instituto de Salud Carlos III (PI17/01067) and AGAUR from the Autonomous Catalan Government (2017SGR1134). Dr. Víctor Antonio Blanco-Palmero is supported by the Instituto de Salud Carlos III (ISCIII, Spanish Biomedical Research Institute) through a “Río Hortega” contract (CM18/0095). Dr. Sara Llamas-Velasco is supported by the Instituto de Salud Carlos III (ISCIII; Spanish Biomedical Research Institute) through a “Juan Rodés” contract (JR 18/00046).S