Eliezer Masliah
National Institutes of Health
1018 Papers
7.3K Citations
Eliezer Masliah is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Neurodegeneration & Biology. The author has an hindex of 170, co-authored 982 publications. Previous affiliations of Eliezer Masliah include University of Miami & Scripps Research Institute.
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Papers
Potential for cell therapy in Parkinson's disease using genetically programmed human embryonic stem cell-derived neural progenitor cells.
Rajesh Ambasudhan,Nima Dolatabadi,Anthony Nutter,Eliezer Masliah,Scott R. McKercher,Stuart A. Lipton +5 more
TL;DR: This review focuses on current state‐of‐the‐art techniques for harnessing hESC‐based strategies toward development of a stem cell therapeutic for Parkinson's disease and describes a novel genetic‐programming approach that may address many of the key challenges that remain in the field and that may hasten clinical translation.
Genetic deletion of Nogo/Rtn4 ameliorates behavioral and neuropathological outcomes in amyloid precursor protein transgenic mice.
Eliezer Masliah,Fang Xie,Shanna Dayan,Edward Rockenstein,Michael Mante,Anthony Adame,Christina Patrick,Andrea F. Chan,Binhai Zheng +8 more
TL;DR: It is found that deleting Nogo ameliorates learning and memory deficits of APP transgenic mice in the Morris water maze at an early/intermediate stage of the disease and these data support the hypothesis that Nogo-mediated inhibition of neuritic sprouting contributes to the disease progression in anAPP transgenic model of AD in a way that is mechanistically distinct from what has been proposed for Rtn3 or NgR.
Mechanisms of cell signaling and inflammation in Alzheimer's disease.
TL;DR: Evidence from tissue culture, in vivo models, and Alzheimer brain tissue studies indicate that inflammation in AD is mediated by the production of proinflammatory molecules, leading to microglial activation and neuronal damage, further supporting a role for inflammation.
Hippocampal neuronal cells that accumulate α-synuclein fragments are more vulnerable to Aβ oligomer toxicity via mGluR5--implications for dementia with Lewy bodies.
Cassia R. Overk,Anna Cartier,Gideon M. Shaked,Edward Rockenstein,Kiren Ubhi,Brian Spencer,Diana L. Price,Christina Patrick,Paula Desplats,Eliezer Masliah +9 more
TL;DR: Together, these results support the possibility that vulnerability of hippocampal neurons to α-syn and Aβ might be mediated via mGluR5 and therapeutical interventions targeting mGLUR5 might have a role in DLB.
Preclinical Assessment of Young Blood Plasma for Alzheimer Disease.
Jinte Middeldorp,Benoit Lehallier,Saul A. Villeda,Suzanne S. M. Miedema,Emily Evans,Eva Czirr,Hui Zhang,Jian Luo,Trisha Stan,Kira I. Mosher,Eliezer Masliah,Tony Wyss-Coray +11 more
TL;DR: Whether young blood plasma ameliorates pathology and cognition in a mouse model for AD and could be a possible future treatment for the disease is investigated.