Moreover, inactivation of the Neu1 gene in the transgenic 5XFAD mice overexpressing human mutant amyloid precursor protein (APP) augmented formation of the plaques whereas intracerebral injections of adeno-associated viruses (AAVs) expressing NEU1 and CTSA could slow down or revert the amyloidogenic process, suggesting that reduced NEU1 brain levels could represent a risk factor for developing Alzheimer disease in humans. The gene discussed is NEU1; the disease is early-onset autosomal dominant Alzheimer disease.