Fig. 5
α-Synuclein, p-tau and amyloid-β pathology load in the anterior insular subregions. α-Synuclein pathology load (n = 23) was significantly higher in DLB agranular insula (5.7%) compared to PD (1.2%) and PDD (2.3%) and in dysgranular insula (3.4%) compared to PD (0.4%) and PDD (0.6%). Log transformation of scores showed significant differences between DLB and PD in agranular insula (P = 0.02) and between DLB and PD as well as PDD in dysgranular insula (P = 0.016 and 0.015; respectively); the agranular insula had significantly higher pathology load (3.25%) compared to the dysgranular insula (1.55%) (a). p-Tau (n = 26) was significantly higher in DLB for both the agranular (41.3%) and dysgranular insula (23.7%) compared to PD (15.1% and 0.25%) and PDD (4% and 0.44%); agranular insula had significantly higher pathology load (18%) compared to the dysgranular insula (7.8%). Amyloid-β (n = 26) was not significantly different between groups but the dysgranular insula had significantly higher pathology load (5%) compared to the agranular insula (3%) (c). Axonal length density (n = 25) based on Bielschowsky silver staining and stereological count showed significantly lower density in the agranular (8 × 10−9 m/m3) compared to the dysgranular insula ( 1 ×10-8 m/m3). The DLB group had significantly lower axonal length density in the agranular insula (6.73 ×10−9 m/m3) compared to the PDD group (9.17 × 10−9 m/m3) and in the dysgranular insula compared to both PD and PDD (11.75 ×10−9 m/m3 and 11.94 × 10−9 m/m3, respectively) (d). Significance: *P < 0.05, **P < 0.01, ***P < 0.001. AD: Alzheimer’s disease; DLB: dementia with Lewy bodies; p-tau: hyperphosphorylated tau; PD: Parkinson’s disease; PDD: Parkinson’s disease dementia