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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

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    Neuroinflammation in Alzheimer's disease.

    Lancet Neurol. 2015 Apr;14(4):388-405

    Authors: Heneka MT, Carson MJ, Khoury JE, Landreth GE, Brosseron F, Feinstein DL, Jacobs AH, Wyss-Coray T, Vitorica J, Ransohoff RM, Herrup K, Frautschy SA, Finsen B, Brown GC, Verkhratsky A, Yamanaka K, Koistinaho J, Latz E, Halle A, Petzold GC, Town T, Morgan D, Shinohara ML, Perry VH, Holmes C, Bazan NG, Brooks DJ, Hunot S, Joseph B, Deigendesch N, Garaschuk O, Boddeke E, Dinarello CA, Breitner JC, Cole GM, Golenbock DT, Kummer MP

    Abstract
    Increasing evidence suggests that Alzheimer's disease pathogenesis is not restricted to the neuronal compartment, but includes strong interactions with immunological mechanisms in the brain. Misfolded and aggregated proteins bind to pattern recognition receptors on microglia and astroglia, and trigger an innate immune response characterised by release of inflammatory mediators, which contribute to disease progression and severity. Genome-wide analysis suggests that several genes that increase the risk for sporadic Alzheimer's disease encode factors that regulate glial clearance of misfolded proteins and the inflammatory reaction. External factors, including systemic inflammation and obesity, are likely to interfere with immunological processes of the brain and further promote disease progression. Modulation of risk factors and targeting of these immune mechanisms could lead to future therapeutic or preventive strategies for Alzheimer's disease.

    PMID: 25792098 [PubMed - as supplied by publisher]

    Adult hippocampal neural stem and progenitor cells regulate the neurogenic niche by secreting VEGF.

    Proc Natl Acad Sci U S A. 2015 Mar 16;

    Authors: Kirby ED, Kuwahara AA, Messer RL, Wyss-Coray T

    Abstract
    The adult hippocampus hosts a population of neural stem and progenitor cells (NSPCs) that proliferates throughout the mammalian life span. To date, the new neurons derived from NSPCs have been the primary measure of their functional relevance. However, recent studies show that undifferentiated cells may shape their environment through secreted growth factors. Whether endogenous adult NSPCs secrete functionally relevant growth factors remains unclear. We show that adult hippocampal NSPCs secrete surprisingly large quantities of the essential growth factor VEGF in vitro and in vivo. This self-derived VEGF is functionally relevant for maintaining the neurogenic niche as inducible, NSPC-specific loss of VEGF results in impaired stem cell maintenance despite the presence of VEGF produced from other niche cell types. These findings reveal adult hippocampal NSPCs as an unanticipated source of an essential growth factor and imply an exciting functional role for adult brain NSPCs as secretory cells.

    PMID: 25775598 [PubMed - as supplied by publisher]

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    Geroscience: linking aging to chronic disease.

    Cell. 2014 Nov 6;159(4):709-13

    Authors: Kennedy BK, Berger SL, Brunet A, Campisi J, Cuervo AM, Epel ES, Franceschi C, Lithgow GJ, Morimoto RI, Pessin JE, Rando TA, Richardson A, Schadt EE, Wyss-Coray T, Sierra F

    Abstract
    Mammalian aging can be delayed with genetic, dietary, and pharmacologic approaches. Given that the elderly population is dramatically increasing and that aging is the greatest risk factor for a majority of chronic diseases driving both morbidity and mortality, it is critical to expand geroscience research directed at extending human healthspan.

    PMID: 25417146 [PubMed - indexed for MEDLINE]