Nevertheless, in parallel to Alzheimer's disease or Parkinson's disease, where soluble forms of amyloid β protein or α‐synuclein are considered to be the toxic species rather than the large aggregated masses of these proteins within plaques or Lewy bodies, it remains possible that soluble monomeric or oligomeric forms of DPR, especially poly‐PR, could, themselves, interfere with TDP‐43 function and RNA metabolism, and in so doing ultimately trigger neurodegeneration. This evidence concerns the gene TARDBP and Alzheimer disease.