{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T17:04:20Z","timestamp":1791219860818,"version":"4.1.0"},"reference-count":19,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2003,7,25]],"date-time":"2003-07-25T00:00:00Z","timestamp":1059091200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[2003,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Decreased levels of \u03b2\u2010amyloid peptide 1\u201042 (A\u03b21\u201042) in cerebrospinal fluid (CSF) are a characteristic feature of Alzheimer's disease (AD) but recently were also observed in Creutzfeldt\u2013Jakob disease (CJD). We analyzed the CSF of patients with CJD, and AD and nondemented controls using a quantitative urea\u2010based A\u03b2 sodium dodecyl sulfate polyacrylamide gel electrophoresis immunoblot. Like in AD and nondemented controls, we found a highly conserved pattern of carboxyterminally truncated A\u03b21\u201037\/38\/39 in addition to A\u03b21\u201040\/42 also in CJD patients. By the introduction of the ratio A\u03b21\u201039 to A\u03b21\u201042, CJD and AD can effectively be differentiated. We conclude that the immunoblot shows disease\u2010specific CSF A\u03b2 peptide patterns in CJD and AD and suppose that measurement of the A\u03b2 peptide pattern seems to be a promising diagnostic tool in the differential diagnosis of dementias. 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