The antibody EM48, used in the cerebral cortex in the present study, detected deposits that were small, nonnuclear and more abundant in patients with Huntington’s disease with increased CAG repeat length, higher Vonsattel grade and earlier age of onset.42 Additionally, colocalization studies did not reveal HTT deposits in microglial or astroglial populations (Fig. 3). This evidence concerns the gene HTT and Huntington disease.