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Recently, neurodegenerative diseases have increasingly been conceptualised as ‘nexopathies’ or disconnection syndromes, in which connectivity changes in neural networks represent the most relevant and characteristic features.1 One of these diseases, behavioural variant frontotemporal dementia (bvFTD), is characterised by morally deviant actions as an early clinical hallmark of this disease, besides other specific changes in personality and behaviour.2 ,3 Elucidating on the neural correlates of these moral impairments contributes to their understanding in this in young patients frequent dementia syndrome and to the understanding of moral actions per se.
One approach towards understanding moral impairments in bvFTD is by comparing affected neural networks in bvFTD with brain networks involved in moral processing in healthy participants during functional imaging studies. Remarkably, this approach enables extraction of new concepts of diseases by using two independent cohorts and imaging methods (lesion studies in disease cohorts vs functional imaging studies in healthy participants).3 Because numerous imaging studies have been published on these issues to date, quantitative meta-analytic approaches are possible.
Accordingly, we combine here two comprehensive quantitative meta-analyses of anatomical and functional neuroimaging data by means of the well-established likelihood estimate method to provide evidence for alterations of regions involved in moral reasoning in bvFTD. Likelihood estimate meta-analyses are based on coordinates of peaks for atrophy or hypometabolism during rest in patients when compared with control participants, or coordinates from functional imaging studies, where …
Contributors MLS planned the design/conceptualisation of the study, analysed and interpreted the data, and drafted and revised the manuscript. DB and SBE contributed to the design/conceptualisation of the study, interpreted the data and revised the manuscript.
JN planned the design/conceptualisation of the study, analysed and interpreted the data, and revised the manuscript.
Funding This work was supported by the Parkinson's Disease Foundation (Grant No. PDF-IRG-1307), MaxNetAging and by LIFE—Leipzig Research Center for Civilization Diseases at the University of Leipzig to MLS. LIFE is funded by means of the European Union, by the European Regional Development Fund (ERFD) and by means of the Free State of Saxony within the framework of the excellence initiative.
Competing interests MLS and JN are supported by the German Federal Ministry of Education and Research (BMBF; German FTLD Consortium, Grant No. FKZ 01GI1007A & FKZ 01EO1001). JN is further supported by the German Research Foundation (SFB 1052 A5). DB is funded by the German National Academic Foundation. SBE acknowledges funding from the National Institute of Health (R01-MH074457-01A1), the German Research Foundation (DFG EI 816/4-1 & LA 3071/3-1), the Helmholtz Initiative on Systems Biology and the European EFT program (Human Brain Project).
Patient consent Obtained.
Ethics approval Ethics committees responsible for single studies (meta-analysis).
Provenance and peer review Not commissioned; externally peer reviewed.
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