Biogen, Citing New Phase 1 Data, Says Aducanumab Reduces Amyloid Plaques in Alzheimer’s

Biogen, Citing New Phase 1 Data, Says Aducanumab Reduces Amyloid Plaques in Alzheimer’s
Aducanamab helps reduce amyloid plaques in Alzheimer's patients who receive a gradually increasing dose of the therapy, its developer, Biogen, reports, citing results from the long-term extension of its ongoing Phase 1b study (NCT01677572). The potential treatment, also known as BIIB037, is a human monoclonal antibody derived from healthy elderly patients who have no signs of cognitive impairment, or from cognitively impaired patients who are declining at an unusually slow rate. Aducanumab is thought to target amyloid plaques — the primary feature of Alzheimer's — based on prior pre-clinical and Phase 1b data. Researchers conducted the Phase 1b clinical trial of aducanumab to assess its effect in patients who received a gradually increasing doses of the drug for up to 24 months, as well as patients given fixed doses of 3, 6 or 10 mg/kg of aducanumab for up to 36 months. Biogen presented data from the study, “Aducanumab titration dosing regimen: 24-month analysis from PRIME: A randomized, double-blind, placebo-controlled Phase 1b study in patients with prodromal or mild Alzheimer’s disease," at the Nov. 1-4 Clinical Trials on Alzheimer’s Disease (CTAD) meeting in Boston. Results from the titration regimen group were consistent with the dose-dependent and time-dependent results seen in patients who received fixed doses of 3, 6 or 10 mg/kg aducanumab during the two-year period. In these patients, amyloid plaque levels — measured by PET scan — decreased in patients upon treatment. Furthermore, the amyloid plaque levels of patients treated with the highest dose declined to levels that were be
Subscribe or to access all post and page content.


  1. Alzheimer’s disease and CADASIL are heritable, adult-onset dementias that both involve damaged small blood vessels.
    As I sit each morning, reading articles in reference to Alzheimer’s I become more discouraged that they haven’t found a treatment or cure for this brain disease after all these years with research and wasted funds.
    Now that Bill Gates is involved let’s hope they make progress for the young ones and get it right.
    Alzheimer’s disease and CADASIL are heritable, adult-onset dementias that both involve damaged small blood vessels.
    Theory #1: With young on set dementia on the rise worldwide. Could the amyloid plaques and tau tangles be connected to a mutation from CADASIL’s, chromosome 19 notch 3 gene. Which is causing the Alzheimer’s brain to go haywire?

    Theory #2: Silent Strokes at any age: Patients unaware they even had one, causes damage to the brain. Affects the thought process, mood, and cognitive functions and may lead to loss of urinary bladder control. So does that mean silent strokes over the years could also lead to young onset dementia?

    This is just a thought: for all medical professionals, be a little more compassionate and inquire about the family history not only physical
    ailments, you need information on the characteristic personality family traits from childhood, which also holds a lot of information. There are more young ones being diagnosed with dementia, it’s not the old person’s disease anymore and you just don’t wake up one day with dementia.

  2. Georges Tony MARCEL,,MD,PhD says:

    It is true that Aducanumab clears amyloid plaques, which is perfecly useless. Adults above 7O frequently have plaques, without Alzheimer!
    The danger of clearing them is freeing small toxic oligomers,which Biogen has NOT disproved.

    Tony Georges MARCEL, MD, PhD

    • Daniel Kidd PhD says:

      The small toxic oligomers are present a decade before cognitive dementia. We need an amyloid beta oligomer biomarker. I was formerly Director of Clinical sample testing for Janssen Alzheimer Immunotherapy. We performed biomarker testing. Individually, I conceived and filed IP for amyloid oligomers, but now, without a lab I need to collaborate with academia, pharma or instrument companies. Hopefully at the Alzheimer Assoc. Intl. Conf in Chicago this month, I’ll make those connections.

Leave a Comment

Your email address will not be published. Required fields are marked *