Skip to main content
Fig. 1 | Translational Neurodegeneration

Fig. 1

From: Axonal degeneration in the anterior insular cortex is associated with Alzheimer’s co-pathology in Parkinson’s disease and dementia with Lewy bodies

Fig. 1

Morphological features of α-synuclein pathology (syn-1) in the anterior insula of PD, PDD and DLB patients. In the agranular insula, LNs in PD_4 (a), a bulgy LN in PDD_1 (b), and LN in layer I in DLB_2 (c). Various LBs were observed in layers 5–6 and intracytoplasmic granular deposits in PD_5 and PD_3 (d,e), an α-synuclein double-string related to a cell, possibly a glial cell, and surrounding a neuronal soma in PDD_1 (f), and circular deposit in DLB_3 (g). Glial synucleinopathy and a long LN (*)  were seen in PDD_1 in deeper layers of agranular insula (h). Vascular synucleinopathy ( *) and glial synucleinopathy were seen in PDD_3 (i,j). In DLB subjects, dense α-synuclein deposits were seen in agranular insula (DLB_8, k), LNs and LBs in the agranular insula in DLB_1 and in the dysgranular insula (l), and star-shaped astrocytic synucleinopathy surrounded by iron deposits (*) in dysgranular insula in DLB_2 (m). Immunoflourescent staining of astroglial synucleinopathy (GFAP in red; α-synuclein in green) in the agranular insula in PD (n), in PDD_1 (o), and in DLB_2 (p) illustrate the extent of glial pathology in PD and DLB. Intensity-based colocalization analysis of GFAP and α-synuclein within same astrocytes shows colocalized voxels (yellow/white pixels; q-s). Magnification (630x), scale bars: 50 μm. DLB: dementia with Lewy bodies; GFAP: glial fibrillary acid protein; LBs: Lewy bodies; LNs: Lewy neurites; PD: Parkinson’s disease; PDD: Parkinson’s disease dementia

Back to article page