Thus, Sho protein is not depleted in Aβ-depositing mice with synaptic damage and hippocampal memory deficits [17], [26], [50], in cuprizone treated mice [31], in mice with a 4-repeat tauopathy [32] and in mice expressing the mutant BRI2 protein of familial Danish dementia [33] (Figure 4). The gene discussed is SPRN; the disease is ITM2B amyloidosis.