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Abstract
Given that extensive cerebral regions are co-atrophic in semantic dementia (SD), it is not yet known which critical regions (SD-semantic-critical regions) are really responsible for the semantic deficits of SD. To identify the SD-semantic-critical regions, we explored the relationship between the degree of cerebral atrophy in the whole brain and the severity of semantic deficits in 19 individuals with SD. We found that the gray matter volumes (GMVs) of two regions [left fusiform gyrus (lFFG) and left parahippocampal gyrus (lPHG)] significantly correlated with the semantic scores of patients with SD. Importantly, the effects of the lFFG remained significant after controlling for the GMVs of the lPHG. Moreover, the effects of the region could not be accounted for by the total GMV, general cognitive ability, laterality of brain atrophy, or control task performance. We further observed that each atrophic portion of the lFFG along the anterior–posterior axis might dedicate to the loss of semantic functions in SD. These results reveal that the lFFG could be a critical region contributing to the semantic deficits of SD.
Highlights
Semantic dementia (SD, which is generally referred to as semantic variant primary progressive aphasia) is characterized by the selective deterioration of semantic knowledge (Snowden et al, 1989; Hodges et al, 1992)
The results revealed that the gray matter volumes (GMVs) values of the left fusiform gyrus (lFFG) still significantly correlated with the semantic principle component analysis (PCA) scores after partialling out the influence of the total GMV (RBA: partial r = 0.84, p < 0.00002; voxel-based analysis (VBA): partial r = 0.92, p < 10−7), general cognitive processing
Atrophy of the lFFG and left parahippocampal gyrus (lPHG) were associated with semantic impairments in semantic dementia (SD), as the reduction of their GMVs significantly correlated to the severity of semantic deficits
Summary
Semantic dementia (SD, which is generally referred to as semantic variant primary progressive aphasia) is characterized by the selective deterioration of semantic knowledge (Snowden et al, 1989; Hodges et al, 1992). The neuroanatomical profile of this disease includes progressive brain atrophy, with the earliest and most severe atrophy occurring in the temporal poles (Mesulam et al, 2012, 2013) These findings promote the assumption that the temporal pole is the critical cortical region responsible for the semantic impairments observed in SD patients (i.e., SD-semantic-critical region; Seeley et al, 2009; Guo et al, 2013). This assumption should be considered with caution given that there are many atrophic cortical regions in SD (i.e., SD-cortical-atrophic regions; Rohrer et al, 2009; La Joie et al, 2014), and some of these regions have been correlated with the severity of semantic deficits in SD (i.e., SD-semantic-correlated regions; Galton et al, 2001; Rosen et al, 2002; Adlam et al, 2006). An SD-semantic-critical region should maintain a significant association with semantic performance in SD after the influence of the other SD-semantic-correlated regions is adjusted
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