It often involves autosomal dominant mutations in genes such as amyloid precursor protein (APP), presenilin 1 (PSEN1), and presenilin2 (PSEN2), which accelerate amyloid-beta accumulation and early pathological changes. Clinically, EOAD progresses rapidly and may present with atypical symptoms such as visuospatial dysfunction, apraxia, or language impairment (Marshe et al., 2019; Rezazadeh et al., 2019; Bertoux et al., 2020; Ramanan et al., 2020; De Felice et al., 2022; Valdez-Gaxiola et al., 2024). This evidence concerns the gene APP and apraxia.