Skip to main content

and
  1. Article

    Open Access

    Characterization of the selective in vitro and in vivo binding properties of crenezumab to oligomeric Aβ

    Accumulation of amyloid β (Aβ) in the brain is proposed as a cause of Alzheimer’s disease (AD), with Aβ oligomers hypothesized to be the primary mediators of neurotoxicity. Crenezumab is a humanized immunoglob...

    William J. Meilandt, Janice A. Maloney, Jose Imperio in Alzheimer's Research & Therapy (2019)

  2. Article

    Open Access

    Structure of Crenezumab Complex with Aβ Shows Loss of β-Hairpin

    Accumulation of amyloid-β (Aβ) peptides and amyloid plaque deposition in brain is postulated as a cause of Alzheimer’s disease (AD). The precise pathological species of Aβ remains elusive although evidence sug...

    Mark Ultsch, Bing Li, Till Maurer, Mary Mathieu, Oskar Adolfsson in Scientific Reports (2016)

  3. No Access

    Article

    A rare mutation in UNC5C predisposes to late-onset Alzheimer's disease and increases neuronal cell death

    Mutations in UNC5C are identified in individuals with late-onset Alzheimer's disease and increase susceptibility of neurons to cell death.

    Monica K Wetzel-Smith, Julie Hunkapiller, Tushar R Bhangale in Nature Medicine (2014)

  4. No Access

    Article

    A mutation in APP protects against Alzheimer’s disease and age-related cognitive decline

    A coding mutation in APP, the gene that encodes the amyloid-β precursor protein, is found to protect against Alzheimer’s disease and cognitive decline in the elderly without Alzheimer’s disease.

    Thorlakur Jonsson, Jasvinder K. Atwal, Stacy Steinberg, Jon Snaedal in Nature (2012)