Eliezer Masliah

Summary

Affiliation: University of California
Country: USA

Publications

  1. Eleuteri S, Di Giovanni S, Rockenstein E, Mante M, Adame A, Trejo M, et al. Novel therapeutic strategy for neurodegeneration by blocking Aβ seeding mediated aggregation in models of Alzheimer's disease. Neurobiol Dis. 2015;74:144-57 pubmed publisher
    ..Together, our findings suggest that targeting fibril growth and Aβ seeding capacity constitutes a viable and effective strategy for protecting against neurodegeneration and disease progression in AD. ..
  2. Rockenstein E, Ubhi K, Mante M, Florio J, Adame A, Winter S, et al. Neuroprotective effects of Cerebrolysin in triple repeat Tau transgenic model of Pick's disease and fronto-temporal tauopathies. BMC Neurosci. 2015;16:85 pubmed publisher
    ..Taken together these results support the notion that CBL may be beneficial in other taupathy models by reducing the levels of aberrantly phosphorylated tau. ..
  3. Spencer B, Valera E, Rockenstein E, Trejo Morales M, Adame A, Masliah E. A brain-targeted, modified neurosin (kallikrein-6) reduces α-synuclein accumulation in a mouse model of multiple system atrophy. Mol Neurodegener. 2015;10:48 pubmed publisher
    ..Thus, the modified, brain-targeted neurosin may warrant further investigation as potential therapy for MSA. ..
  4. Koob A, Shaked G, Bender A, Bisquertt A, Rockenstein E, Masliah E. Neurogranin binds α-synuclein in the human superior temporal cortex and interaction is decreased in Parkinson's disease. Brain Res. 2014;1591:102-10 pubmed publisher
  5. Mandler M, Valera E, Rockenstein E, Mante M, Weninger H, Patrick C, et al. Active immunization against alpha-synuclein ameliorates the degenerative pathology and prevents demyelination in a model of multiple system atrophy. Mol Neurodegener. 2015;10:10 pubmed publisher
    ..This study further validates the efficacy of vaccination with AFFITOPEs® for ameliorating the neurodegenerative pathology in synucleinopathies. ..
  6. Valera E, Masliah E. Therapeutic approaches in Parkinson's disease and related disorders. J Neurochem. 2016;139 Suppl 1:346-352 pubmed publisher
    ..This article is part of a special issue on Parkinson disease. ..
  7. Kim C, Ojo Amaize E, Spencer B, Rockenstein E, Mante M, Desplats P, et al. Hypoestoxide reduces neuroinflammation and α-synuclein accumulation in a mouse model of Parkinson's disease. J Neuroinflammation. 2015;12:236 pubmed publisher
    ..These results support the therapeutic potential of HE for PD and other α-synuclein-related diseases. ..
  8. Overk C, Rockenstein E, Florio J, Cheng Q, Masliah E. Differential calcium alterations in animal models of neurodegenerative disease: Reversal by FK506. Neuroscience. 2015;310:549-60 pubmed publisher
    ..The coupling of two-photon microscopy data and statistical classifiers serves to effectively create a bioassay where the number of animals and scientific resources can be reduced without compromising the results of the experiment. ..
  9. Rockenstein E, Desplats P, Ubhi K, Mante M, Florio J, Adame A, et al. Neuro-peptide treatment with Cerebrolysin improves the survival of neural stem cell grafts in an APP transgenic model of Alzheimer disease. Stem Cell Res. 2015;15:54-67 pubmed publisher
    ..These results suggest that CBL might protect grafted NSCs and as such be a potential adjuvant therapy when combined with grafting. ..

More Information

Publications34

  1. Valera E, Mante M, Anderson S, Rockenstein E, Masliah E. Lenalidomide reduces microglial activation and behavioral deficits in a transgenic model of Parkinson's disease. J Neuroinflammation. 2015;12:93 pubmed publisher
    ..These results support the therapeutic potential of lenalidomide for reducing maladaptive neuroinflammation in PD and related neuropathologies. ..
  2. Spencer B, Potkar R, Metcalf J, Thrin I, Adame A, Rockenstein E, et al. Systemic Central Nervous System (CNS)-targeted Delivery of Neuropeptide Y (NPY) Reduces Neurodegeneration and Increases Neural Precursor Cell Proliferation in a Mouse Model of Alzheimer Disease. J Biol Chem. 2016;291:1905-20 pubmed publisher
    ..Overall, increased delivery of NPY to the CNS for AD might be an effective therapy especially if combined with an anti-Aβ therapeutic. ..
  3. Fields J, OVERK C, Adame A, Florio J, Mante M, Pineda A, et al. Neuroprotective effects of the immunomodulatory drug FK506 in a model of HIV1-gp120 neurotoxicity. J Neuroinflammation. 2016;13:120 pubmed publisher
    ..Together, these results suggest that FK506 might be potentially neuroprotective in patients with HAND by mitigating inflammation and mitochondrial alterations. ..
  4. de Wilde M, Overk C, Sijben J, Masliah E. Meta-analysis of synaptic pathology in Alzheimer's disease reveals selective molecular vesicular machinery vulnerability. Alzheimers Dement. 2016;12:633-44 pubmed publisher
  5. Gillman A, Lee J, Ramachandran S, Capone R, Gonzalez T, Wrasidlo W, et al. Small molecule NPT-440-1 inhibits ionic flux through A?1-42 pores: Implications for Alzheimer's disease therapeutics. Nanomedicine. 2016;12:2331-2340 pubmed publisher
    ..Combined with previous studies on site-specific amino acid substitutions, these results suggest that pharmacological modulation of A?1-42 could prevent amyloid pore-mediated AD pathogenesis. ..
  6. Wrasidlo W, Tsigelny I, Price D, Dutta G, Rockenstein E, Schwarz T, et al. A de novo compound targeting ?-synuclein improves deficits in models of Parkinson's disease. Brain. 2016;139:3217-3236 pubmed
  7. Rockenstein E, Ubhi K, Trejo M, Mante M, Patrick C, Adame A, et al. Cerebrolysin™ efficacy in a transgenic model of tauopathy: role in regulation of mitochondrial structure. BMC Neurosci. 2014;15:90 pubmed publisher
  8. Kim C, Rockenstein E, Spencer B, Kim H, Adame A, Trejo M, et al. Antagonizing Neuronal Toll-like Receptor 2 Prevents Synucleinopathy by Activating Autophagy. Cell Rep. 2015;13:771-782 pubmed publisher
    ..These results uncover roles of TLR2 in regulating neuronal autophagy and suggest that the TLR2 pathway may be targeted for autophagy activation strategies in treating neurodegenerative disorders. ..
  9. FIELDS J, Serger E, Campos S, Divakaruni A, Kim C, SMITH K, et al. HIV alters neuronal mitochondrial fission/fusion in the brain during HIV-associated neurocognitive disorders. Neurobiol Dis. 2016;86:154-69 pubmed publisher
    ..Promoting mitochondrial fission during HIV infection of the CNS may restore mitochondrial biogenesis and prevent neurodegeneration. ..
  10. Spencer B, Kim C, Gonzalez T, Bisquertt A, Patrick C, Rockenstein E, et al. α-Synuclein interferes with the ESCRT-III complex contributing to the pathogenesis of Lewy body disease. Hum Mol Genet. 2016;25:1100-15 pubmed publisher
    ..Better understanding of the mechanisms of intracellular trafficking of α-syn might be important for understanding the pathogenesis and developing new treatments for synucleinopathies. ..
  11. request reprint
    Masliah E, Hansen L, Adame A, Crews L, Bard F, Lee C, et al. Abeta vaccination effects on plaque pathology in the absence of encephalitis in Alzheimer disease. Neurology. 2005;64:129-31 pubmed
    ..This case illustrates the effects of an Abeta-based immunization on AD pathogenesis in the absence of overt meningoencephalitis and leukoencephalopathy. ..
  12. Valera E, Spencer B, Fields J, Trinh I, Adame A, Mante M, et al. Combination of alpha-synuclein immunotherapy with anti-inflammatory treatment in a transgenic mouse model of multiple system atrophy. Acta Neuropathol Commun. 2017;5:2 pubmed publisher
    ..These results suggest that a strategic combination of treatments may improve the therapeutic outcome in trials for MSA and related neurodegenerative disorders. ..
  13. request reprint
    Masliah E, Rockenstein E, Veinbergs I, Mallory M, Hashimoto M, Takeda A, et al. Dopaminergic loss and inclusion body formation in alpha-synuclein mice: implications for neurodegenerative disorders. Science. 2000;287:1265-9 pubmed
    ..These results suggest that accumulation of wild-type alpha-synuclein may play a causal role in Parkinson's disease and related conditions. ..
  14. Dhungel N, Eleuteri S, Li L, Kramer N, Chartron J, Spencer B, et al. Parkinson's disease genes VPS35 and EIF4G1 interact genetically and converge on α-synuclein. Neuron. 2015;85:76-87 pubmed publisher
    ..Finally, we provide a resource of candidate PD genes for future interrogation. ..
  15. Spencer B, Desplats P, Overk C, Valera Martin E, Rissman R, Wu C, et al. Reducing Endogenous α-Synuclein Mitigates the Degeneration of Selective Neuronal Populations in an Alzheimer's Disease Transgenic Mouse Model. J Neurosci. 2016;36:7971-84 pubmed publisher
  16. Buxbaum J, Roberts A, Adame A, Masliah E. Silencing of murine transthyretin and retinol binding protein genes has distinct and shared behavioral and neuropathologic effects. Neuroscience. 2014;275:352-64 pubmed publisher
    ..This is the first description of behavioral abnormalities in Rbp4(-/-)mice. The data also indicate that it is unlikely that the behaviors seen in Ttr(-/-) mice are related to its function as an RBP carrier. ..
  17. OVERK C, Rockenstein E, Valera E, Stefanova N, Wenning G, Masliah E. Multiple system atrophy: experimental models and reality. Acta Neuropathol. 2018;135:33-47 pubmed publisher
  18. Fields J, Metcalf J, OVERK C, Adame A, Spencer B, Wrasidlo W, et al. The anticancer drug sunitinib promotes autophagyand protects from neurotoxicity in an HIV-1 Tat model of neurodegeneration. J Neurovirol. 2017;23:290-303 pubmed publisher
    ..We conclude that sunitinib might ameliorate Tat-mediated autophagy alterations and may decrease neurodegeneration in aging patients with HAND. ..
  19. FIELDS J, Dumaop W, Crews L, Adame A, Spencer B, Metcalf J, et al. Mechanisms of HIV-1 Tat neurotoxicity via CDK5 translocation and hyper-activation: role in HIV-associated neurocognitive disorders. Curr HIV Res. 2015;13:43-54 pubmed
    ..g.: Tau, CRMP2, DCX] that impair neuronal function and eventually lead to cell death. Novel therapeutic approaches with compounds that block Tat mediated hyper-activation of CDK5 might be of value in the management of HAND. ..
  20. Fields J, Dumaop W, Eleuteri S, Elueteri S, Campos S, Serger E, et al. HIV-1 Tat alters neuronal autophagy by modulating autophagosome fusion to the lysosome: implications for HIV-associated neurocognitive disorders. J Neurosci. 2015;35:1921-38 pubmed publisher
    ..Therapies targeting Tat-mediated autophagy alterations may decrease neurodegeneration in aging patients with HAND. ..
  21. Games D, Valera E, Spencer B, Rockenstein E, Mante M, Adame A, et al. Reducing C-terminal-truncated alpha-synuclein by immunotherapy attenuates neurodegeneration and propagation in Parkinson's disease-like models. J Neurosci. 2014;34:9441-54 pubmed publisher
  22. Overk C, Masliah E. Pathogenesis of synaptic degeneration in Alzheimer's disease and Lewy body disease. Biochem Pharmacol. 2014;88:508-16 pubmed publisher
  23. Crews L, Ruf R, Patrick C, Dumaop W, Trejo Morales M, Achim C, et al. Phosphorylation of collapsin response mediator protein-2 disrupts neuronal maturation in a model of adult neurogenesis: Implications for neurodegenerative disorders. Mol Neurodegener. 2011;6:67 pubmed publisher
    ..We have developed an in vitro model of abnormal CDK5 activation during adult hippocampal neurogenesis, and here we used this model to investigate aberrantly phosphorylated downstream targets of CDK5...
  24. Masliah E, Rockenstein E, Mante M, Crews L, Spencer B, Adame A, et al. Passive immunization reduces behavioral and neuropathological deficits in an alpha-synuclein transgenic model of Lewy body disease. PLoS ONE. 2011;6:e19338 pubmed publisher
    ..These results suggest that passive immunization with monoclonal antibodies against the CT of ?-syn may be of therapeutic relevance in patients with PD and DLB...
  25. Masliah E, Rockenstein E, Veinbergs I, Sagara Y, Mallory M, Hashimoto M, et al. beta-amyloid peptides enhance alpha-synuclein accumulation and neuronal deficits in a transgenic mouse model linking Alzheimer's disease and Parkinson's disease. Proc Natl Acad Sci U S A. 2001;98:12245-50 pubmed
    ..Therefore, treatments that block the production or accumulation of beta-amyloid peptides could benefit a broader spectrum of disorders than previously anticipated. ..