Skip to main content
Fig. 10 | Acta Neuropathologica Communications

Fig. 10

From: ApoER2-Dab1 disruption as the origin of pTau-associated neurodegeneration in sporadic Alzheimer’s disease

Fig. 10

Dab1 accumulates together with ApoER2 signaling partners in LC and raphe nucleus in sAD. A Serial transverse sections of the upper pons from representative non-AD control (Braak stage I) and sAD (Braak stage V) cases were probed with antibodies targeting ApoER2-Dab1 pathway components (see Additional file 1: Table S3). In the non-sAD controls (A), single-target IHC revealed that Dab1 is expressed by a subset of LC and raphe nucleus neurons (solid arrows in A3, A5) and their neuritic projections (open arrows in A3, A5). pTauSer202/Thr205 and pPSD95Thr19 accumulated within small subsets of LC and raphe nucleus neurons (solid arrows in A8–10). pTauSer202/Thr205 also accumulated in neuritic projections (open arrows in A8) while pPSD95 accumulated as discrete punctae in adjacent neuropil (open arrows in A8). In sAD cases (B), prominent accumulations of Dab1 were observed within clusters of globular structures (open arrows in B2–10) and as inclusions within abnormal neurons (solid arrows in B9). Additional examples of intraneuronal Dab1 inclusions are provided in Additional file 1: Ext Fig. S10.1 C Dab1 accumulated across the clinicopathological spectrum of sAD and correlated with Braak stage. For dot plots, p values are from Kruskal–Wallis tests. The fitted line plot shows Spearman’s rank correlation coefficients and p values. D MP-IHC suggested that Dab1, pTauSer202/Thr205, and pPSD95Thr19 accumulate within the same ApoER2-expressing neurons (D1–4) and appeared to accumulate within MAP2-positive dendritic arbors (white circles in E1–4). Scale bars in MP-IHC images = 10 µm

Back to article page