Genomes and Genes
Affiliation: Nathan Kline Institute
- Cystatin C: a potential target for Alzheimer's treatmentEfrat Levy
Expert Rev Neurother 8:687-9. 2008
- The role of cystatin C in cerebral amyloid angiopathy and stroke: cell biology and animal modelsEfrat Levy
Department of Psychiatry, New York University School of Medicine, and Nathan Kline Institute, Orangeburg 10962, USA
Brain Pathol 16:60-70. 2006..This review focuses on cell culture and animal models used to study the role of cystatin C in these processes...
- Studies on the first described Alzheimer's disease amyloid beta mutant, the Dutch variantEfrat Levy
Department of Pharmacology, New York University School of Medicine, New York, New York, USA
J Alzheimers Dis 9:329-39. 2006..However, most AD patients have no genetic defects in AbetaPP, indicating that other factors may alter Abeta production, conformation, and/or clearance initiating the disease process...
- Binding of cystatin C to Alzheimer's amyloid beta inhibits in vitro amyloid fibril formationMagdalena Sastre
Departments of Pharmacology, New York University School of Medicine, 550 First Avenue, New York, NY, 10016, USA
Neurobiol Aging 25:1033-43. 2004..Notably, cystatin C association with Abeta results in a concentration-dependent inhibition of Abeta fibril formation...
- Immunization targeting a minor plaque constituent clears β-amyloid and rescues behavioral deficits in an Alzheimer's disease mouse modelJose Morales-Corraliza
Center for Dementia Research, Nathan S Kline Institute for Psychiatric Research, Orangeburg, NY 10962, USA
Neurobiol Aging 34:137-45. 2013....
- Neuronal apoptosis and autophagy cross talk in aging PS/APP mice, a model of Alzheimer's diseaseDun Sheng Yang
Center for Dementia Research, Nathan Kline Institute, New York University School of Medicine, 140 Old Orangeburg Rd, Bldg 39, Orangeburg, NY 10962, USA
Am J Pathol 173:665-81. 2008..Our findings establish apoptosis as a mode of neuronal cell death in aging PS/APP mice and identify the cross talk between autophagy and apoptosis, which influences neuronal survival in AD-related neurodegeneration...
- Days to criterion as an indicator of toxicity associated with human Alzheimer amyloid-beta oligomersSam Gandy
Department of Neurology, Mount Sinai School of Medicine, New York, NY 10029, USA
Ann Neurol 68:220-30. 2010..We sought to study the bioactivities of endogenously formed oAbeta/ADDLs generated in situ from the physiological processing of human amyloid precursor protein (APP) and presenitin1 (PS1) transgenes...
- In vitro assays measuring protection by proteins such as cystatin C of primary cortical neuronal and smooth muscle cellsSebastien A Gauthier
Department of Psychiatry, New York University School of Medicine, New York, NY, USA
Methods Mol Biol 849:275-87. 2012..The effect of endogenous level of cystatin C expression is studied by comparing stressed primary cells isolated from brains of cystatin C transgenic, cystatin C knockout, and wild-type mice...
- Complexes of amyloid-beta and cystatin C in the human central nervous systemWeiqian Mi
Nathan S Kline Institute, Orangeburg, New York, USA
J Alzheimers Dis 18:273-80. 2009..Thus, enhancing CysC expression or modulating CysC binding to Abeta have important disease-modifying effects, suggesting a novel therapeutic intervention for AD...
- In vivo turnover of tau and APP metabolites in the brains of wild-type and Tg2576 mice: greater stability of sAPP in the beta-amyloid depositing miceJose Morales-Corraliza
Nathan Kline Institute for Psychiatric Research, Orangeburg, New York, USA
PLoS ONE 4:e7134. 2009..Given the neurotrophic roles attributed to sAPP, the enhanced stability of sAPP in the beta-amyloid depositing Tg2576 mice may represent a neuroprotective response...
- Purification of human wild-type or variant cystatin C from conditioned media of transfected cellsFrances Prelli
Department of Pathology, New York University School of Medicine, NY, USA
Methods Mol Biol 299:221-6. 2005..Following native purification conditions, variant cystatin C has a distinct structure compared to the wild-type protein...
- Therapeutic effects of remediating autophagy failure in a mouse model of Alzheimer disease by enhancing lysosomal proteolysisDun Sheng Yang
Nathan Kline Institute, Orangeburg, NY, USA
Autophagy 7:788-9. 2011..Our findings underscore the pathogenic significance of autophagic-lysosomal dysfunction in AD and demonstrate the value of reversing this dysfunction as an innovative therapeautic strategy for AD...
- Olfactory dysfunction correlates with amyloid-beta burden in an Alzheimer's disease mouse modelDaniel W Wesson
Emotional Brain Institute and Center for Dementia Research, Nathan S Kline Institute for Psychiatric Research, Orangeburg, New York 10962, USA
J Neurosci 30:505-14. 2010..Furthermore, these results present the odor cross-habituation test as a powerful behavioral assay, which reflects Abeta deposition and thus may serve to monitor the efficacy of therapies aimed at reducing Abeta...
- Age-dependent dysregulation of brain amyloid precursor protein in the Ts65Dn Down syndrome mouse modelJennifer H K Choi
Center for Dementia Research, Nathan Kline Institute, Orangeburg, New York 10962, USA
J Neurochem 110:1818-27. 2009..Therefore, multiple mechanisms contribute to the regulation towards diploid levels of APP metabolites in the Ts65Dn mouse brain...
- Reversal of autophagy dysfunction in the TgCRND8 mouse model of Alzheimer's disease ameliorates amyloid pathologies and memory deficitsDun Sheng Yang
Center for Dementia Research, Nathan Kline Institute, Orangeburg, NY 10962, USA
Brain 134:258-77. 2011..Our findings support the pathogenic significance of autophagic-lysosomal dysfunction in Alzheimer's disease and indicate the potential value of restoring normal autophagy as an innovative therapeutic strategy for Alzheimer's disease...
- Systemic pathology in aged mouse models of Down's syndrome and Alzheimer's diseaseSeymour Levine
Center for Dementia Research, Nathan S Kline Institute, 140 Old Orangeburg Road, Orangeburg, NY 10962, USA
Exp Mol Pathol 86:18-22. 2009..The occurrence of lymphomas in mouse DS models is of interest in relation to the increased incidence of malignant conditions in human DS...
- Proteins that bind to the RERMS region of beta amyloid precursor proteinMonika Pawlik
Nathan Kline Institute, 140 Old Orangeburg Road, Orangeburg, NY 10962, USA
Biochem Biophys Res Commun 355:907-12. 2007..Because both APP and hCRMP-2 promote neuronal outgrowth and use a common signaling pathway, APP could be acting through a semaphorin receptor as well...
- Mechanisms of neural and behavioral dysfunction in Alzheimer's diseaseDaniel W Wesson
Emotional Brain Institute, Nathan S Kline Institute for Psychiatric Research, New York University School of Medicine, Orangeburg, NY 10962, USA
Mol Neurobiol 43:163-79. 2011....
- Overexpression of human cystatin C in transgenic mice does not affect levels of endogenous brain amyloid Beta PeptideMonika Pawlik
Department of Pharmacology, New York University School of Medicine, New York, NY, 10016, USA
J Mol Neurosci 22:13-8. 2004..Thus, in vivo overexpression of human cystatin C does not affect Abeta levels in mice that do not deposit Abeta...
- Murine cerebrovascular cells as a cell culture model for cerebral amyloid angiopathy: isolation of smooth muscle and endothelial cells from mouse brainSebastien A Gauthier
Department of Psychiatry, New York University School of Medicine, New York, NY, USA
Methods Mol Biol 849:261-74. 2012..Finally, we compare our methods with protocols designed to isolate and maintain human cerebrovascular cell cultures...
- Cystatin C inhibits amyloid-beta deposition in Alzheimer's disease mouse modelsWeiqian Mi
Nathan S Kline Institute, Orangeburg, New York 10962, USA
Nat Genet 39:1440-2. 2007..Thus, cystatin C has a protective role in Alzheimer's disease pathogenesis, and modulation of cystatin C concentrations may have therapeutic implications for the disease...
- Alzheimer's presenilin 1 modulates sorting of APP and its carboxyl-terminal fragments in cerebral neurons in vivoSam Gandy
Farber Institute for Neurosciences and the Department of Neurology, Thomas Jefferson University, Philadelphia, Pennsylvania, USA
J Neurochem 102:619-26. 2007..The chimera experiment suggests that TGN-enrichment of a beta-/gamma-secretase substrate may play an integral role in the action of mutant PS1 to elevate brain levels of Abeta42...
- Cystatin C modulates cerebral beta-amyloidosisStephan A Kaeser
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Otfried Muller Strasse 27, D 72076 Tubingen, Germany
Nat Genet 39:1437-9. 2007..Our results suggest that cystatin C concentrations modulate cerebral amyloidosis risk and provide an opportunity for genetic risk assessment and therapeutic interventions...
- Murine cerebrovascular cells as a cell culture model for cerebral amyloid angiopathy: isolation of smooth muscle and endothelial cells from mouse brainSonia S Jung
Center for Dementia Research, Nathan S. Kline Institute for Psychiatric Research, Orangeburg, NY, USA
Methods Mol Biol 299:211-9. 2005....
- Animal models for cerebral amyloid angiopathyEfrat Levy; Fiscal Year: 2006..The proposed animal models are crucial for understanding the etiology of cerebral amyloid angiopathy and hemorrhage and for the development of rational therapeutic interventions. ..
- BETAAPP MODULATION BY THE ADAPTER PROTEINS FE65 AND X11Efrat Levy; Fiscal Year: 2003..Manipulating the interaction of Beta-APP with an effector protein, such as X11 or Fe65, may provide a novel approach for the pharmacological modulation of Beta-APP processing in Alzheimer's disease. ..