{"id":12894,"date":"2024-05-06T14:28:19","date_gmt":"2024-05-06T14:28:19","guid":{"rendered":"https:\/\/www.drknowhk.org\/?p=12894"},"modified":"2024-06-27T14:30:51","modified_gmt":"2024-06-27T14:30:51","slug":"alzheimers-variant-may-cause-distinct-form-of-the-disease","status":"publish","type":"post","link":"http:\/\/www.drknowhk.org\/mo\/alzheimers-variant-may-cause-distinct-form-of-the-disease\/","title":{"rendered":"Alzheimer’s Variant May Cause Distinct Form of the Disease"},"content":{"rendered":"

\u5c0d\u4e0d\u8d77\uff0c\u6b64\u5185\u5bb9\u53ea\u9069\u7528\u65bcEnglish<\/a>\u3002<\/p>

By Judy George<\/p>\n

Source: medpagetoday<\/p>\n

The APOE4<\/em> variant may be more than just a genetic risk factor for Alzheimer’s disease, new data from several cohorts suggested.<\/p>\n

Clinical, pathological, and biomarker changes indicated that APOE<\/em>4 homozygotes may have a distinct, genetically determined form of Alzheimer’s, according to Juan Fortea, MD, PhD, of the Hospital of Sant Pau in Barcelona, Spain, and co-authors.<\/p>\n

In an analysis spanning several cohorts, almost all APOE4<\/em> homozygotes had Alzheimer’s pathology and significantly higher levels of Alzheimer’s biomarkers from age 55 compared with APOE3<\/em> homozygotes. By age 65, nearly all had abnormal cerebrospinal fluid (CSF) levels, and 75% had positive amyloid scans, Fortea and colleagues reported in Nature Medicine<\/em>opens in a new tab or window<\/span>. The prevalence of these markers increased with age, reaching almost full penetrance over time.<\/p>\n