{
  "abstract": "Australia has approved controversial Alzheimer’s drug lecanemab after two rejections.1 The amyloid hypothesis posits that amyloid is the cause of Alzheimer’s disease and underpins claims that anti-amyloid antibodies such as lecanemab and donanemab are “disease modifying.”23 The implication is that these agents are superior to current options. But numerous trials targeting amyloid have failed to show meaningful clinical improvement.45 Although lecanemab and donanemab reliably clear plaques and yield small statistical signals on cognitive scales,23 these changes have not translated into a truly substantial functional benefit. Lecanemab, for example, slowed decline on the clinical dementia rating-sum of boxes (CDR-SB) scale by only 0.45 points over 18 months,2 and donanemab by 0.67 points in people with low or medium tau pathology,3 which are both below the levels of change that Andrews et al estimated may represent a meaningful decline within patients (around 1-2 points on the CDR-SB).6 An alternative explanation, more parsimonious with the data, is that amyloid is not the ultimate driver of disease and that these antibodies are therefore not truly disease modifying.45789",
  "authors": [
    {
      "affiliations": [
        "Neuroscience and Regenerative Medicine, St Vincent’s Hospital Centre for Applied Medical Research, Darlinghurst, Sydney, NSW, Australia"
      ],
      "name": "Bryce Vissel"
    }
  ],
  "title": "Anti-amyloid antibodies for Alzheimer’s disease are not truly disease modifying",
  "uid": "f8fa6489-08d9-5ff1-b78f-4b3c9bc440a2"
}