A recent study reported that parietal WMH pathogenesis in AD is related to axonal loss, through Wallerian-like degeneration, which corresponds to cortical phosphorylated tau burden, and demyelination in patients with AD but to vasculopathy and ischemia (by sclerotic index as a marker of small vessel disease and myelin associated glycoprotein to proteolipid protein ratio as a measure of hypoperfusion) in individuals without AD, suggesting that some degree of WMH is secondary to neurodegeneration in the context of AD [57]. The gene discussed is MAG; the disease is Alzheimer disease.