Extended Data Fig. 12: NPTX2 immunofluorescence in brain sections of patients with neurodegenerative proteinopathies.
From: A model of human neural networks reveals NPTX2 pathology in ALS and FTLD
Additional immunofluorescence gallery of multiple FTLD, ALS and AD cases demonstrating NPTX2 accumulation and inclusions in neurons with TDP-43p403/404-positive aggregates in the hippocampus of (a) FTLD-TDP-A cases, (b) FTLD-TDP-C case and in the primary motor cortex of an ALS case (c). d, Note that while the NPTX2 pathology could be observed in cortex of both FTLD-TDP and ALS patients, it is only present when the TDP-43p403/404-positive aggregate-containing neurons could still be identified by the MAP2 staining (right) as opposed to the disintegrated, “ghost neurons” that left behind only the TDP-43p403/404-positive aggregates (left). Absence of NPTX2 accumulation in neurons with FUS or taup202/205 inclusions in FTLD-FUS hippocampus (e) or FTLD-tau frontal cortex (f), respectively. NPTX2 aberrancy is absent from neurons with taup202/205-positive (g, h lower panels) but present in neurons with TDP-43p403/404-positive (h upper panels) inclusions in the hippocampus of AD cases. Patient IF was repeated 4 (FTLD-TDP-A and -C cases) or 2 times (FTLD-FUS, FTLD-tau, AD, ALS cases). Scale bars, (a,b,d-h) 10 µm, (c) 20 µm.
