To determine if GDE2 disruption contributes to TDP-43 abnormalities in disease, we took advantage of earlier observations that GDE2 aberrantly accumulates in intracellular compartments of patients with AD, ALS, and ALS/FTD (GDE2acc) (Nakamura et al, 2021; Westerhaus et al, 2022). This evidence concerns the gene TARDBP and amyotrophic lateral sclerosis.