In contrast, in PSP, the main feature is the presence of neurofibrillary tangles predominantly composed of hyperphosphorylated tau, compromising considerably different brain structures.21 Hence, as CRH is decreased to a similar extent in PSP and MSA, and it was not altered when comparing SAA− to SAA+ Alzheimer’s disease/frontotemporal dementia/vascular dementia, an αSyn-independent mechanism might be behind the decrease of CRH levels in these diseases. This evidence concerns the gene CRH and Alzheimer disease.