Extended Data Fig. 12: NPTX2 immunofluorescence in brain sections of patients with neurodegenerative proteinopathies.

Additional immunofluorescence gallery of multiple FTLD, ALS and AD cases demonstrating NPTX2 accumulation and inclusions in neurons with TDP-43^p403/404-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-43^p403/404-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-43^p403/404-positive aggregates (left). Absence of NPTX2 accumulation in neurons with FUS or tau^p202/205 inclusions in FTLD-FUS hippocampus (e) or FTLD-tau frontal cortex (f), respectively. NPTX2 aberrancy is absent from neurons with tau^p202/205-positive (g, h lower panels) but present in neurons with TDP-43^p403/404-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.