Disrupted Face Processing in Frontotemporal Dementia: A Review of the Clinical and Neuroanatomical Evidence
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Faces play an integral role in day-to-day functioning, particularly for social interactions where dynamic and rapid processing of information is vital. Analysis of faces allows an individual to ascertain a wide range of information including deciphering mood and identity, with these assessments directing an individual’s subsequent response and behaviours. The prominent social and emotional deficits observed in frontotemporal dementia (FTD), a younger-onset dementia syndrome, may in part reflect a breakdown of the face processing network. Different subtypes of FTD present with divergent patterns of atrophy, although damage is predominantly confined to the frontal and temporal lobes. Specific predictions regarding the role of frontal and temporal regions in face processing have been proposed in the model outlined by Haxby et al. Trends in Cognitive Sciences, 4(6), 223–233 (2000). This model presents a parsimonious method by which to understand face processing in FTD while concurrently allowing assessment of the predictive value and applicability of such a model. By applying the Haxby model to the existing FTD literature, this review presents both direct and indirect evidence of a breakdown in key elements of the face processing network. The type and degree of breakdown appears to differ as a function of FTD subtype and associated brain atrophy. The evidence presented in this review and its relationship with predictions of the Haxby model provides impetus and direction for future research investigating face processing in FTD.
KeywordsBehavioural-variant frontotemporal dementia Semantic dementia Progressive nonfluent aphasia Emotion Identity Neuroimaging
Acknowledgements and Funding
This work was supported by funding to ForeFront, a collaborative research group dedicated to the study of frontotemporal dementia and motor neuron disease, from the National Health and Medical Research Council of Australia (NHMRC) Research Project Grant (APP1037746) and the Australia Research Council (ARC) Centre of Excellence in Cognition and its Disorders Memory Node (CE11000102). R.H. is supported by an Australian Postgraduate Award. O.P. is supported by an NHMRC Senior Research Fellowship (APP1103258) F.K. is supported by an NHMRC-ARC Dementia Research Development Fellowship (APP1097026).
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