This is via mutations in VAPB (ALS, PD) (Nishimura et al., 2004a; Kun-Rodrigues et al., 2015), disruption of VAPB’s interaction with PTPIP51 and hence ER-mitochondria contacts (ALS, AD, and PD via α-Synuclein binding, seeTable 1) (Paillusson et al., 2017; Lau et al., 2020; Gómez-Suaga et al., 2022) or reduced VAPB levels (ALS, AD, MSA) (Anagnostou et al., 2010; Lau et al., 2020; Mori et al., 2021). This evidence concerns the gene RMDN3 and Alzheimer disease.