For instance, although [11C]Martinostat uptake in DLB and PD was increased in primary motor cortex, consistent with PD postmortem studies demonstrating histone altered HDAC expression in that region,(29) alpha-synuclein pathology in this region is usually only a late manifestation of disease.(34) Thus, not all changes in class HDAC I density that we observed are likely to be a cell autonomous response to alpha-synuclein pathology. This evidence concerns the gene SNCA and Parkinson disease.