David Harrison
Takeda Cambridge LtdCambridge
331254 RESULTS
Takeda Cambridge LtdCambridge
Universidade de AveiroAveiro, Portugal
ANTIBODY monoclonal 6D11 laboratory 6D11<br />(R.J. Kascsak, Department of Neurology, New York University School of Medicine, New York, NY<br />Paper, <a href="http://www.jleukbio.org/cgi/content/full/81/6/1374" target="_new">
COMMENT The results described are surprising, and do not readily fit with the work from Mucke's group on fyn. It is also amazing how the loss of STEP corrects the behavioral impairment, without modifying the underlying pathology at all—at least at this early
COMMENT Zhang et al. have published a very interesting study showing that deletion of the striatal-enriched tyrosine phosphatase (STEP) gene protects the 3xTg animal model of Alzheimer disease. The interesting part of this study is that the protection is not at t
PAPER Laird AS, Van Hoecke A, De Muynck L, Timmers M, Van Den Bosch L, Van Damme P, Robberecht W
PAPER Bekenstein U, Kadener S
PAPER Ginhoux F, Greter M, Leboeuf M, Nandi S, See P, Gokhan S, Mehler MF, Conway SJ, Ng LG, Stanley ER, Samokhvalov IM, Merad M
PAPER Vergani F, Landi A, Pirillo D, Cilia R, Antonini A, Sganzerla EP
PAPER Zhivotovsky B, Orrenius S
PAPER Mastroberardino PG, Piacentini M
PAPER Shao JL, Wan XH, Chen Y, Bi C, Chen HM, Zhong Y, Heng XH, Qian JQ
PAPER Liu G, Guo H, Guo C, Zhao S, Gong D, Zhao Y
RESEARCH NEWS 2010-10-24 Research News Could the field be one step closer to a new potential therapy for Alzheimer disease? Possibly, if the target is striatal-enriched tyrosine phosphatase (STEP). Deletion of this gene restored cognition and repaired synapses in AD transgenic mi
PAPER Binolfi A, Rodriguez EE, Valensin D, D'Amelio N, Ippoliti E, Obal G, Duran R, Magistrato A, Pritsch O, Zweckstetter M, Valensin G, Carloni P, Quintanar L, Griesinger C, Fernández CO
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