This year’s MetLife Foundation Awards for Medical Research go to two researchers well known to Alzforum: Randall Bateman of Washington University School of Medicine, St. Louis, and Christian Haass of Ludwig Maximilians University and the German Center for Neurodegenerative Diseases, both in Munich. Each receives a $150,000 institutional grant and a $50,000 personal prize. The two winners will be announced this morning at a plenary session of the Alzheimer’s Association International Conference, which runs until July 23 in Washington, D.C.

Bateman studies biomarkers of neurodegenerative diseases. He pioneered a method called stable isotope-linked kinetics, or SILK, that measures the generation of Aβ in the central nervous system (Jun 2006 news). This led to the discovery that patients with sporadic Alzheimer’s disease poorly clear the peptide from the brain, while people with familial Alzheimer’s disease make more of it (Jul 2010 newsJun 2013 news). SILK helps scientists estimate the efficacy of anti-amyloid therapies. Bateman is now working on a similar method to measure tau in cerebrospinal fluid. He also directs the Dominantly Inherited Alzheimer’s Network Trial Unit (DIAN-TU), which evaluates the safety and efficacy of the anti-amyloid antibodies gantenerumab and solanezumab in non-symptomatic people carrying an autosomal dominant mutation.  

Haass studies the molecular pathologies of neurodegenerative disease, including Alzheimer’s, frontotemporal lobar degeneration, and amyotrophic lateral sclerosis (ALS). He was among the first to report that cells produce Aβ under healthy conditions (Haass et al., 1992). More recently, he found that β-secretase is essential for myelination in the peripheral nervous system, raising concerns about targeting the enzyme as a therapeutic strategy (May 2013 news). He also investigates how mutations in TREM2 and C9ORF72 increase risk for AD and ALS, respectively (see Kleinberger et al., 2014Alzforum Webinar; Feb 2013 news).

Bateman and Hass will receive their awards tonight at the Marriott Marquis Hotel in Washington, D.C., Salon 9, beginning at 6. They will briefly present their work in a session moderated by David Holtzman from WashU.—Gwyneth Dickey Zakaib


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News Citations

  1. CSF Aβ—New Approach Shows Rapid Flux, May Help Evaluate Therapeutics
  2. Honolulu: Wake-Up Call—Aβ Clearance, Not Production, Awry in AD
  3. In Familial AD, Aβ Production Up, Clearance Down
  4. Paracrine Signal From BACE1-Clipped Neuregulin Rescues Myelin
  5. RNA Twist: C9ORF72 Intron Expansion Makes Aggregating Protein

Therapeutics Citations

  1. Gantenerumab
  2. Solanezumab

Webinar Citations

  1. Mutations Impair TREM2 Maturation, Processing, and Microglial Phagocytosis

Paper Citations

  1. . Amyloid beta-peptide is produced by cultured cells during normal metabolism. Nature. 1992 Sep 24;359(6393):322-5. PubMed.
  2. . TREM2 mutations implicated in neurodegeneration impair cell surface transport and phagocytosis. Sci Transl Med. 2014 Jul 2;6(243):243ra86. PubMed.

External Citations

  1. DIAN-TU

Further Reading


  1. . Age and amyloid effects on human central nervous system amyloid-beta kinetics. Ann Neurol. 2015 Sep;78(3):439-53. Epub 2015 Jul 20 PubMed.
  2. . Amyloid-β efflux from the central nervous system into the plasma. Ann Neurol. 2014 Dec;76(6):837-44. Epub 2014 Oct 24 PubMed.
  3. . Amyloid-β diurnal pattern: possible role of sleep in Alzheimer's disease pathogenesis. Neurobiol Aging. 2014 Sep;35 Suppl 2:S29-34. Epub 2014 May 15 PubMed.
  4. . TREM2 mutations implicated in neurodegeneration impair cell surface transport and phagocytosis. Sci Transl Med. 2014 Jul 2;6(243):243ra86. PubMed.
  5. . Cellular mechanisms of ALS mutations - a loss or a gain of function?. Drug Res (Stuttg). 2013 Nov;63 Suppl 1:S17. Epub 2013 Nov 15 PubMed.
  6. . Loss of ALS-associated TDP-43 in zebrafish causes muscle degeneration, vascular dysfunction, and reduced motor neuron axon outgrowth. Proc Natl Acad Sci U S A. 2013 Mar 26;110(13):4986-91. PubMed.