Since soluble Aβo start to accumulate in the brain up to two decades before the appearance of clinical symptoms (Cline et al., 2018), understanding how Aβ pathology disturbs cell functioning and neuronal networks would be exceedingly beneficial to develop novel therapeutic approaches to prevent memory deficits at the onset of AD before neurodegeneration induces irreversible brain damages that drastically compromises the quality of life of the patient. The gene discussed is ABO; the disease is Alzheimer disease.