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Front. Aging Neurosci. | doi: 10.3389/fnagi.2018.00300

Commentary: Cerebellar atrophy and its contribution to cognition in frontotemporal dementias

  • 1Laboratory of Experimental Psychology and Neuroscience, Institute of Cognitive and Translational Neuroscience (INCYT), Argentina

Commentary: Cerebellar atrophy and its contribution to cognition in frontotemporal dementias


Agustín Ibáñez1,2,3,4,5,*, Adolfo M. García1,2,6

1 Institute of Cognitive and Translational Neuroscience (INCYT), INECO Foundation, Favaloro University, Buenos Aires, Argentina

2 National Scientific and Technical Research Council (CONICET), Buenos Aires, Argentina

3 Center for Social and Cognitive Neuroscience (CSCN), School of Psychology, Universidad Adolfo Ibanez, Santiago, Chile

4 Universidad Autónoma del Caribe, Barranquilla, Colombia

5 Centre of Excellence in Cognition and its Disorders, Australian Research Council (ACR), Sydney, Australia

6 Facultad de Educación, Universidad Nacional de Cuyo, Mendoza, Argentina

*correspondence: aibanez@ineco.org.ar


Commentary: Cerebellar atrophy and its contribution to cognition in frontotemporal dementias


Comment on: Yu Chen MD Fiona Kumfor PhD Ramon Landin‐Romero PhD Muireann Irish PhD John R. Hodges MD, FRCP Olivier Piguet PhD. Cerebellar atrophy and its contribution to cognition in frontotemporal dementias. 2018. https://doi.org/10.1002/ana.25271


The embodied little brain: From neurocognition to neurodegeneration

Cheng et al.[1] provide unprecedented evidence of syndrome-specific changes in cerebellar grey matter integrity (mainly in lobules VI, Crus I and Crus II) across three frontotemporal dementia (FTD) subtypes, alongside specific associations with attentional, visuospatial, mnesic, and language-motor deficits. Moreover, results survived covariation with each group’s distinctive atrophy pattern. These outcomes illuminate the critical role of the cerebellum in non-motor processes, while highlighting the relevance of distributed network approaches to cognitive (dys)function.
Although the cerebellum has been implicated in higher-order domains[2; 3; 4], including executive functions, language, interoception, and social cognition, these results may prove surprising to many clinical neuroscientists. Indeed, the cerebellum remains notably underexplored within neurocognitive assessments of dementia, where it is still largely conceived as a specifically motoric region and is thus often excluded from imaging analyses seeking to map brain-behavior associations. Similarly, except for research on ataxia, systematic assessments of regional and network-level alterations involving the cerebellum are wanting in the field. This counterproductive neglect, we believe, stems from a dissociation between dementia studies and current neurocognitive theories [5].
Fertile ground could be gained by anchoring neurodegeneration research on the embodied cognition approach, which has revealed multidimensional links between action-related circuits and higher-order functions. The cerebellum, as a core hub in these cortical-subcortical networks, would play an important, enactive role in several cognitive processes. While lesion and agenesia studies suggest that this role may not be causal, cerebellar circuits have been directly implicated in embodied domains[6; 7; 8; 9]. Beyond the field’s traditional focus on canonical atrophy patterns and selected cognitive skills, emerging evidence suggests that diffuse neurocognitive dysfunctions are partially overlapped across dementias. The profuse interconnectedness, functional richness, and transdiagnostic vulnerability of the cerebellum render it a key target to examine embodied cognitive deficits in FTD and other conditions.
Accordingly, embodied theories of the cerebellum could become critical tools to foster relevant translational developments. First, they underscore the need to systematically report cerebellar involvement in diverse neurocognitive deficits. Also, they provide a profitable platform to track intercognitive phenomena –enactive synergies among varied psychobiological (dys)functions– from a network-based perspective[5; 10; 11; 12]. Moreover, they promote a reinterpretation of symptoms from an action-grounded neurocognitive rationale[13]. These milestones could have direct clinical implications, as the lack of proper theoretical frameworks can lead to neglecting, downplaying, or delaying the report of cerebellar disturbances across pathologies. We call for novel studies integrating embodied, intercognitive, network-based conceptualizations of the cerebellum to foster translational breakthroughs in dementia research.

Keywords: Cerebellum, Frontotemperal lobar degeneration, Cognition, imaging, Language, social cognition

Received: 20 Aug 2018; Accepted: 13 Sep 2018.

Edited by:

Ashok Kumar, University of Florida, United States

Reviewed by:

Ignacio Torres-Aleman, Consejo Superior de Investigaciones Científicas (CSIC), Spain  

Copyright: © 2018 Ibanez and García. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Dr. Agustin Ibanez, Institute of Cognitive and Translational Neuroscience (INCYT), Laboratory of Experimental Psychology and Neuroscience, Buenos Aires, Argentina, aibanez@ineco.org.ar