For example, low CSF Aβ1‐42 levels have been related to disease severity and clinical progression in multiple sclerosis45 and Lewy body disease (Parkinson’s disease and Lewy body dementia).46 In addition, the CSF levels of Aβ1‐42 have been found decreased in neuropathologically confirmed cases of Creutzfeldt–Jakob disease independently of cerebral amyloid deposition47 and in neuroinfectious diseases.48 This evidence supports the view that the CSF levels of APP‐derived peptides could reflect pathophysiological mechanisms other than cerebral amyloid deposition.10 Here, APP is linked to Parkinson disease.