Interestingly, removing the muscarinic M1 receptor in the 3xTgAD and Tg-SwDI mice (two models relevant to AD) by crossbreeding them with M(1)R(−/−) mice worsened their cognitive impairments and elevated plaque and tangle levels in the brains of the 3xTgAD mice and enhanced the cerebrovascular deposition of fibrillar Aβ in the Tg-SwDI mice [48], substantiating the role of disturbed M1 receptors (deletion or antagonism) in increasing Aβ production and exacerbating the AD pathology. The gene discussed is CHRM1; the disease is Alzheimer disease.