The insoluble Aβ concentration in brain homogenates also was increased (p = 0.009) (Fig. 7B) and we found that the ratio of MAG:PLP1 correlated inversely with insoluble Aβ (r = −0.59, p = 0.06, Fig. 7C), providing evidence that the chronic hypoperfusion in AD is explained in part by increased Aβ. The gene discussed is PLP1; the disease is Alzheimer disease.