Activity of smooth muscle actin (SMA) was reduced in the brains of patients with late stage AD, while increased arteriolar SMA expression together with frequent Aβ plaques observed in the brains of non-demented subjects suggests that increased SMA expression might represent a physiological response to neurodegeneration that could prevent or delay the onset of clinical dementia in subjects with cerebral AD neuropathology [67]. The gene discussed is SMN1; the disease is dementia.