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Lab News

03-02-15 Joe wins 2015 New Vision Award
Joe had a very successful conference last week, and was awarded the 2015 New Vision Award at the Charleston Conference on Alzheimer’s disease. This is a highly selective award (with money!) which involves a first round of selections to attend the conference and then a study section-like discussion of the remaining entries at the conference. Joe’s proposal was selected unanimously.
01-27-15 Tony speaks at World Economic Forum
Tony was invited to Davos to discuss how to tackle brain diseases at the World Economic Forum!
12-02-14 Final round for Breakthrough of the Year!
We made the final round for Science's 2014 Breakthrough of the year!  Let everyone know so they can vote!
11-13-14 Vote for the breakthrough of the year!
Help us win Sciene Breakthrough of 2014 by voting for "Young blood fixes old."
09-23-14 Creative Minds: Tony and Tom are in the news!
Congratulations to Tony and Tom for being in the NIH Director's blog.  You can read it here!

pubmed: wyss-coray

    Related Articles

    TREM2 mutations implicated in neurodegeneration impair cell surface transport and phagocytosis.

    Sci Transl Med. 2014 Jul 2;6(243):243ra86

    Authors: Kleinberger G, Yamanishi Y, Suárez-Calvet M, Czirr E, Lohmann E, Cuyvers E, Struyfs H, Pettkus N, Wenninger-Weinzierl A, Mazaheri F, Tahirovic S, Lleó A, Alcolea D, Fortea J, Willem M, Lammich S, Molinuevo JL, Sánchez-Valle R, Antonell A, Ramirez A, Heneka MT, Sleegers K, van der Zee J, Martin JJ, Engelborghs S, Demirtas-Tatlidede A, Zetterberg H, Van Broeckhoven C, Gurvit H, Wyss-Coray T, Hardy J, Colonna M, Haass C

    Abstract
    Genetic variants in the triggering receptor expressed on myeloid cells 2 (TREM2) have been linked to Nasu-Hakola disease, Alzheimer's disease (AD), Parkinson's disease, amyotrophic lateral sclerosis, frontotemporal dementia (FTD), and FTD-like syndrome without bone involvement. TREM2 is an innate immune receptor preferentially expressed by microglia and is involved in inflammation and phagocytosis. Whether and how TREM2 missense mutations affect TREM2 function is unclear. We report that missense mutations associated with FTD and FTD-like syndrome reduce TREM2 maturation, abolish shedding by ADAM proteases, and impair the phagocytic activity of TREM2-expressing cells. As a consequence of reduced shedding, TREM2 is virtually absent in the cerebrospinal fluid (CSF) and plasma of a patient with FTD-like syndrome. A decrease in soluble TREM2 was also observed in the CSF of patients with AD and FTD, further suggesting that reduced TREM2 function may contribute to increased risk for two neurodegenerative disorders.

    PMID: 24990881 [PubMed - indexed for MEDLINE]