Neuroinflammation and oxidative stress have both been linked to neuroaxonal injury, gliosis and proteopathies.66 Moreover, lack of elevated plasma NfL, GFAP and tau in our sample suggests that white matter changes might not be progressive in our sample, or indeed confounded by proteins stemming from the periphery rather than the brain.67 Once again, a longitudinal examination is required to ascertain whether the relationship between plasma markers and white matter microarchitecture is associated with subsequent white and grey matter neurodegeneration. The gene discussed is MAPT; the disease is proteostasis deficiencies.