Familial Alzheimer’s disease (fAD) is an autosomal dominant, early-onset form of Alzheimer’s disease (AD), commonly caused by mutations in PSEN1. Among these, the PSEN1 M146L variant is one of the most frequently reported pathogenic mutations and has been associated with aggressive disease progression. Despite its prevalence, the functional consequences of this mutation remain poorly understood, particularly in underrepresented populations such as those from Latin America. To address this gap, we generated a human induced pluripotent stem cell (hiPSC) line from erythroblasts amplified from peripheral blood mononuclear cells of an Argentine patient clinically diagnosed with fAD and carrying the heterozygous PSEN1 p.M146L variant. Reprogramming was performed using the STEMCCA lentiviral vector, which encodes the Yamanaka factors (OCT4, KLF4, SOX2, and c-MYC). The resulting hiPSC line, named FBAD1, exhibited typical pluripotent morphology and expressed endogenous markers (OCT4, SOX2, NANOG, and TRA-1-60), as validated by immunofluorescence and RT-qPCR. FBAD1 also showed differentiation into the three germ layers by embryoid body assay, maintained a normal karyotype, and carried the PSEN1 M146L variant, confirmed by Sanger sequencing. Importantly, directed differentiation yielded cortical and glutamatergic neurons, validated by neuronal and subtype-specific markers. This hiPSC line represents a patient-specific model to identify early pathogenic signatures associated with AD.