Peter Davies

Summary

Affiliation: North Shore University Hospital
Country: USA

Publications

  1. pmc Neuronal c-Abl activation leads to induction of cell cycle and interferon signaling pathways
    Sarah D Schlatterer
    Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    J Neuroinflammation 9:208. 2012
  2. pmc Mechanism-based treatments for Alzheimer's disease
    Peter Davies
    Litwin Zucker Center for Research on Alzheimer s Disease, Feinstein Institute for Medical Research, Manhasset, NY 11030, USA
    Dialogues Clin Neurosci 11:159-69. 2009
  3. pmc CALHM1 P86L polymorphism modulates CSF Aβ levels in cognitively healthy individuals at risk for Alzheimer's disease
    Jeremy Koppel
    Litwin Zucker Research Center for the Study of Alzheimer s Disease, The Feinstein Institute for Medical Research, Manhasset, New York, USA
    Mol Med 17:974-9. 2011
  4. ncbi request reprint Cell-cycle reentry and cell death in transgenic mice expressing nonmutant human tau isoforms
    Cathy Andorfer
    Department of Neuroscience, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    J Neurosci 25:5446-54. 2005
  5. pmc Identification of potent small-molecule inhibitors of STAT3 with anti-inflammatory properties in RAW 264.7 macrophages
    Hemachander Capiralla
    Litwin Zucker Research Center for the Study of Alzheimer s Disease, Feinstein Institute for Medical Research, Manhasset, NY 11030, USA
    FEBS J 279:3791-9. 2012
  6. pmc Tau phosphorylated at tyrosine 394 is found in Alzheimer's disease tangles and can be a product of the Abl-related kinase, Arg
    Matthew A Tremblay
    Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    J Alzheimers Dis 19:721-33. 2010
  7. pmc Mice devoid of Tau have increased susceptibility to neuronal damage in myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis
    Jason G Weinger
    Department of Pathology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    J Neuropathol Exp Neurol 71:422-33. 2012
  8. pmc Small-molecule activators of AMP-activated protein kinase (AMPK), RSVA314 and RSVA405, inhibit adipogenesis
    Valérie Vingtdeux
    Litwin Zucker Research Center for the Study of Alzheimer s Disease, The Feinstein Institute for Medical Research, Manhasset, New York, USA
    Mol Med 17:1022-30. 2011
  9. doi request reprint CALHM1 controls the Ca²⁺-dependent MEK, ERK, RSK and MSK signaling cascade in neurons
    Ute Dreses-Werringloer
    Litwin Zucker Research Center for the Study of Alzheimer s Disease, The Feinstein Institute for Medical Research, Manhasset, New York, USA
    J Cell Sci 126:1199-206. 2013
  10. pmc AMP-activated protein kinase signaling activation by resveratrol modulates amyloid-beta peptide metabolism
    Valérie Vingtdeux
    Litwin Zucker Research Center for the Study of Alzheimer s Disease, The Feinstein Institute for Medical Research, North Shore LIJ, Manhasset, New York 11030, USA
    J Biol Chem 285:9100-13. 2010

Collaborators

Detail Information

Publications49

  1. pmc Neuronal c-Abl activation leads to induction of cell cycle and interferon signaling pathways
    Sarah D Schlatterer
    Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    J Neuroinflammation 9:208. 2012
    ....
  2. pmc Mechanism-based treatments for Alzheimer's disease
    Peter Davies
    Litwin Zucker Center for Research on Alzheimer s Disease, Feinstein Institute for Medical Research, Manhasset, NY 11030, USA
    Dialogues Clin Neurosci 11:159-69. 2009
    ..It is as yet unclear which, if any, of these approaches will be successful, but the high level of activity in each of these three fields provides some hope that an effective treatment for Alzheimer's disease is on the horizon...
  3. pmc CALHM1 P86L polymorphism modulates CSF Aβ levels in cognitively healthy individuals at risk for Alzheimer's disease
    Jeremy Koppel
    Litwin Zucker Research Center for the Study of Alzheimer s Disease, The Feinstein Institute for Medical Research, Manhasset, New York, USA
    Mol Med 17:974-9. 2011
    ..These data further demonstrate the utility of endophenotype-based approaches focusing on CSF biomarkers for the identification or validation of risk factors for AD...
  4. ncbi request reprint Cell-cycle reentry and cell death in transgenic mice expressing nonmutant human tau isoforms
    Cathy Andorfer
    Department of Neuroscience, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    J Neurosci 25:5446-54. 2005
    ....
  5. pmc Identification of potent small-molecule inhibitors of STAT3 with anti-inflammatory properties in RAW 264.7 macrophages
    Hemachander Capiralla
    Litwin Zucker Research Center for the Study of Alzheimer s Disease, Feinstein Institute for Medical Research, Manhasset, NY 11030, USA
    FEBS J 279:3791-9. 2012
    ....
  6. pmc Tau phosphorylated at tyrosine 394 is found in Alzheimer's disease tangles and can be a product of the Abl-related kinase, Arg
    Matthew A Tremblay
    Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    J Alzheimers Dis 19:721-33. 2010
    ..Given the reported role of Arg in oxidative stress response and neural development, the ability to phosphorylate tau at Y394 implicates Arg as a potential player in the pathogenesis of Alzheimer's disease and other tauopathies...
  7. pmc Mice devoid of Tau have increased susceptibility to neuronal damage in myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis
    Jason G Weinger
    Department of Pathology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    J Neuropathol Exp Neurol 71:422-33. 2012
    ....
  8. pmc Small-molecule activators of AMP-activated protein kinase (AMPK), RSVA314 and RSVA405, inhibit adipogenesis
    Valérie Vingtdeux
    Litwin Zucker Research Center for the Study of Alzheimer s Disease, The Feinstein Institute for Medical Research, Manhasset, New York, USA
    Mol Med 17:1022-30. 2011
    ..This work shows that the novel small-molecule activators of AMPK (RSVA314 and RSVA405) are potent inhibitors of adipogenesis and thus may have therapeutic potential against obesity...
  9. doi request reprint CALHM1 controls the Ca²⁺-dependent MEK, ERK, RSK and MSK signaling cascade in neurons
    Ute Dreses-Werringloer
    Litwin Zucker Research Center for the Study of Alzheimer s Disease, The Feinstein Institute for Medical Research, Manhasset, New York, USA
    J Cell Sci 126:1199-206. 2013
    ..The present study identifies a previously uncharacterized mechanism of control of Ca(2+)-dependent ERK1/2 signaling in neurons, and further establishes CALHM1 as a critical ion channel for neuronal signaling and function...
  10. pmc AMP-activated protein kinase signaling activation by resveratrol modulates amyloid-beta peptide metabolism
    Valérie Vingtdeux
    Litwin Zucker Research Center for the Study of Alzheimer s Disease, The Feinstein Institute for Medical Research, North Shore LIJ, Manhasset, New York 11030, USA
    J Biol Chem 285:9100-13. 2010
    ..These data suggest that resveratrol and pharmacological activation of AMPK have therapeutic potential against Alzheimer disease...
  11. pmc Age-dependent impairment of cognitive and synaptic function in the htau mouse model of tau pathology
    Manuela Polydoro
    Dominick P Purpura Department of Neuroscience, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    J Neurosci 29:10741-9. 2009
    ..Our results suggest that tau pathology may underlie an age-dependent learning impairment through disruption of synaptic function...
  12. ncbi request reprint The familial dementia BRI2 gene binds the Alzheimer gene amyloid-beta precursor protein and inhibits amyloid-beta production
    Shuji Matsuda
    Albert Einstein College of Medicine, Bronx, NY 10461, USA
    J Biol Chem 280:28912-6. 2005
    ..Finding that BRI2 pathogenic mutations alter the regulatory function of BRI2 on A(beta)PP processing would define dysregulation of A(beta)PP cleavage as a pathogenic mechanism common to AD, FDD, and FBD...
  13. pmc AMPK is abnormally activated in tangle- and pre-tangle-bearing neurons in Alzheimer's disease and other tauopathies
    Valérie Vingtdeux
    Litwin Zucker Research Center for the Study of Alzheimer s Disease, The Feinstein Institute for Medical Research, North Shore LIJ, 350 Community Drive, Manhasset, NY 11030, USA
    Acta Neuropathol 121:337-49. 2011
    ..By controlling tau phosphorylation, AMPK might regulate neurodegeneration and therefore could represent a novel common determinant in tauopathies...
  14. pmc Gas1 interferes with AβPP trafficking by facilitating the accumulation of immature AβPP in endoplasmic reticulum-associated raft subdomains
    Julien Chapuis
    Litwin Zucker Research Center for the Study of Alzheimer s Disease, The Feinstein Institute for Medical Research, Manhasset, NY 11030, USA
    J Alzheimers Dis 28:127-35. 2012
    ..Together these data show that Gas1 interfered with AβPP trafficking by interacting with AβPP to facilitate its translocation into specialized ER-associated rafts where immature AβPP accumulated...
  15. pmc Performance-based measures of everyday function in mild cognitive impairment
    Terry E Goldberg
    Litwin Zucker Center for Research in Alzheimer s Disease and Memory Disorders, Feinstein Institute for Medical Research, 350 Community Dr, Manhassett, NY 11030, USA
    Am J Psychiatry 167:845-53. 2010
    ....
  16. doi request reprint Relationships between behavioral syndromes and cognitive domains in Alzheimer disease: the impact of mood and psychosis
    Jeremy Koppel
    The Litwin Zucker Research Center for the Study of Alzheimer s Disease and Memory Disorders, The Feinstein Institute for Medical Research, The North Shore Long Island Jewish Health System, Manhasset, NY, USA
    Am J Geriatr Psychiatry 20:994-1000. 2012
    ....
  17. pmc c-Abl in neurodegenerative disease
    Sarah D Schlatterer
    Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    J Mol Neurosci 45:445-52. 2011
    ..Based on this evidence, a potential role for c-Abl in the pathogenesis of neurodegenerative disease is discussed, and we attempt to place activation of c-Abl in context with other known contributors to neurodegenerative pathology...
  18. pmc Neuronal c-Abl overexpression leads to neuronal loss and neuroinflammation in the mouse forebrain
    Sarah D Schlatterer
    Department of Pathology, Albert Einstein College of Medicine, Bronx, NY, USA
    J Alzheimers Dis 25:119-33. 2011
    ..Given the evidence of c-Abl activation in the human AD brain combined with the pathological phenotype of AblPP/tTA mice, it is likely that aberrant c-Abl activity may play a role in neurodegenerative disease...
  19. pmc Differential incorporation of tau isoforms in Alzheimer's disease
    Marisol Espinoza
    Department of Pathology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Forchheimer 526, Bronx, NY 10461, USA
    J Alzheimers Dis 14:1-16. 2008
    ....
  20. pmc Novel synthetic small-molecule activators of AMPK as enhancers of autophagy and amyloid-β peptide degradation
    Valérie Vingtdeux
    Litwin Zucker Research Center for the Study of Alzheimer s Disease, Feinstein Institute for Medical Research, North Shore Long Island Jewish Medical Center, Manhasset, New York, NY 11030, USA
    FASEB J 25:219-31. 2011
    ..This work identifies the RSVA compounds as promising lead molecules for the development of a new class of AMPK activating drugs controlling mTOR signaling, autophagy, and Aβ clearance...
  21. pmc Therapeutic potential of resveratrol in Alzheimer's disease
    Valérie Vingtdeux
    Litwin Zucker Research Center for the Study of Alzheimer s Disease, The Feinstein Institute for Medical Research, North Shore LIJ, Manhasset, NY 11030, USA
    BMC Neurosci 9:S6. 2008
    ..Furthermore, recent work in cell cultures and animal models has shed light on the molecular mechanisms potentially involved in the beneficial effects of resveratrol intake against the neurodegenerative process in Alzheimer's disease...
  22. pmc MAPT isoforms: differential transcriptional profiles related to 3R and 4R splice variants
    Shufen Chen
    The Litwin Zucker Research Center for Study of Alzheimer s Disease, The Feinstein Institute for Medical Research, North Shore University Hospital, Manhasset, NY 11030, USA
    J Alzheimers Dis 22:1313-29. 2010
    ..Our data add to complex findings on the role of 3R/4R in normal and abnormal neuronal function and highlight several molecular mechanisms that might drive neurodegeneration, or perhaps, set the stage for it...
  23. pmc Anesthesia-induced hyperphosphorylation detaches 3-repeat tau from microtubules without affecting their stability in vivo
    Emmanuel Planel
    Taub Institute for Alzheimer s Disease Research, Department of Pathology, Columbia University Medical Center, New York, New York 10032, USA
    J Neurosci 28:12798-807. 2008
    ..Tau remaining on the MTs under these conditions is sufficient to maintain MT network integrity...
  24. ncbi request reprint Molecular evolution and genetics of the Saitohin gene and tau haplotype in Alzheimer's disease and argyrophilic grain disease
    Chris Conrad
    Department of Pathology, Albert Einstein College of Medicine, Bronx, New York, USA
    J Neurochem 89:179-88. 2004
    ..More detailed studies confirm the H2 haplotype to be the ancestral tau gene. This situation is reminiscent of the evolution of the apolipoprotein (ApoE) gene, another locus that is potentially important for the risk of development of AD...
  25. pmc Methods for measuring tau pathology in transgenic mouse models
    Stefanie K Forest
    Department of Pathology, Albert Einstein College of Medicine, Bronx, NY, USA
    J Alzheimers Dis 33:463-71. 2013
    ..In addition the new monoantibody ELISA offers a simple quantitative method to measure the amount of aggregated tau in both human and mouse brains...
  26. ncbi request reprint Semantic distance abnormalities in mild cognitive impairment: their nature and relationship to function
    Brady C Kirchberg
    Litwin Zucker Center for Research in Alzheimer s Disease and Memory Disorders, Feinstein Institute for Medical Research, Manhasset, NY, USA
    Am J Psychiatry 169:1275-83. 2012
    ..The authors sought to directly examine compromises in the semantic system in mild cognitive impairment and their possible relationship to everyday functional competencies...
  27. ncbi request reprint A long trek down the pathways of cell death in Alzheimer's disease
    Peter Davies
    Department of Pathology, Albert Einstein College of Medicine, 1300 Morris Park Ave, Bronx, NY 10461, USA
    J Alzheimers Dis 9:265-9. 2006
    ..This brief and personal description of my laboratory's search for the cause of cell dysfunction and death in Alzheimer's disease marks only highlights, and my apologies to those whose work I have passed over...
  28. ncbi request reprint Hyperphosphorylation and aggregation of tau in mice expressing normal human tau isoforms
    Cathy Andorfer
    Departments of Neuroscience and Pathology, Albert Einstein College of Medicine, Bronx, New York, USA
    J Neurochem 86:582-90. 2003
    ..This pathologic tau accumulates in the cell bodies and dendrites of neurons in a spatiotemporally relevant distribution...
  29. pmc Sensitive quantitative assays for tau and phospho-tau in transgenic mouse models
    Christopher M Acker
    Department of Pathology, Albert Einstein College of Medicine, Bronx, NY, USA
    Neurobiol Aging 34:338-50. 2013
    ..Taken together, these assays are valuable methods to quantify tau and phospho-tau levels in transgenic animals, by examining tau levels in brain and measuring tau as a potential serum biomarker...
  30. ncbi request reprint Troglitazone, a peroxisome proliferator-activated receptor-gamma agonist, decreases tau phosphorylation in CHOtau4R cells
    Cristina d'Abramo
    Department of Pathology, Albert Einstein College of Medicine, Bronx, New York 10461, USA
    J Neurochem 98:1068-77. 2006
    ..Thus, we believe that the thiazolidinedione regulates tau phosphorylation through a PPARgamma-dependent/independent mechanism involving an Akt/glycogen synthase kinase-3(GSK-3beta)-independent signalling cascade: PDK1/p70S6K/mTor...
  31. pmc An Open-Label Exploratory Study with Memantine: Correlation between Proton Magnetic Resonance Spectroscopy and Cognition in Patients with Mild to Moderate Alzheimer's Disease
    Marc L Gordon
    The Litwin Zucker Research Center, The Feinstein Institute for Medical Research, Manhasset, N Y, USA
    Dement Geriatr Cogn Dis Extra 2:312-20. 2012
    ..To characterize progression of Alzheimer's disease (AD) using proton magnetic resonance spectroscopy ((1)H MRS)...
  32. pmc Resveratrol mitigates lipopolysaccharide- and Aβ-mediated microglial inflammation by inhibiting the TLR4/NF-κB/STAT signaling cascade
    Hemachander Capiralla
    The Litwin Zucker Research Center for the Study of Alzheimer s Disease, The Feinstein Institute for Medical Research, Manhasset, New York, USA
    J Neurochem 120:461-72. 2012
    ..Further studies in cell culture systems showed that resveratrol acted via a mechanism involving the TLR4/NF-κB/STAT signaling cascade...
  33. pmc Growth arrest-specific 1 binds to and controls the maturation and processing of the amyloid-beta precursor protein
    Julien Chapuis
    Litwin Zucker Research Center for the Study of Alzheimer s Disease, The Feinstein Institute for Medical Research, North Shore LIJ, Manhasset, NY 11030, USA
    Hum Mol Genet 20:2026-36. 2011
    ..These results suggest that Gas1 is a novel APP-interacting protein involved in the control of APP maturation and processing...
  34. pmc Effects of cell cycle inhibitors on tau phosphorylation in N2aTau3R cells
    Concepcion Conejero-Goldberg
    The Litwin Zucker Research Center for Study of Alzheimer s Disease, The Feinstein Institute for Medical Research, North Shore University Hospital, 350 Community Drive, Manhasset, NY 11030, USA
    J Mol Neurosci 35:143-50. 2008
    ..These results are also in agreement with the lack of phosphorylation seen for cisplatin, another inhibitor that produces disruption of the MT-dynamics...
  35. pmc Tau passive immunotherapy in mutant P301L mice: antibody affinity versus specificity
    Cristina d'Abramo
    Litwin Zucker Center for Research in Alzheimer s Disease, Feinstein Institute for Medical Research, North Shore LIJ Health System, Manhasset, New York, United States of America
    PLoS ONE 8:e62402. 2013
    ..These data demonstrate that passive immunotherapy in mutant tau models may be efficacious in reducing the development of tau pathology, but a great deal of work remains to be done to carefully select the tau epitopes to target...
  36. doi request reprint CB2 Receptor Deficiency Increases Amyloid Pathology and Alters Tau Processing in a Transgenic Mouse Model of Alzheimer's Disease
    Jeremy Koppel
    Litwin Zucker Research Center, Feinstein Institute for Medical Research, North Shore Long Island Jewish Health System, Manhasset, New York, United States of America
    Mol Med 19:357-64. 2013
    ....
  37. doi request reprint Development and cross-validation of the UPSA short form for the performance-based functional assessment of patients with mild cognitive impairment and Alzheimer disease
    Jesús J Gomar
    Litwin Zucker Alzheimer s Disease Center, Feinstein Institute, Manhassett, NY, USA
    Am J Geriatr Psychiatry 19:915-22. 2011
    ..It has been found that patients with cognitive impairment have daily living functional skills altered at very early stages of illness...
  38. pmc Correlation of Alzheimer disease neuropathologic changes with cognitive status: a review of the literature
    Peter T Nelson
    Sanders Brown Center on Aging, Department of Pathology, University of Kentucky, Lexington 40536 0230, USA
    J Neuropathol Exp Neurol 71:362-81. 2012
    ..Although Aβ plaques may play a key role in AD pathogenesis, the severity of cognitive impairment correlates best with the burden of neocortical neurofibrillary tangles...
  39. pmc Endocannabinoids in Alzheimer's disease and their impact on normative cognitive performance: a case-control and cohort study
    Jeremy Koppel
    The Litwin Zucker Research Center for the Study of Alzheimer s Disease and Memory Disorders, The Feinstein Institute for Medical Research, Manhasset, NY 11030, USA
    Lipids Health Dis 8:2. 2009
    ..To date, no published studies have investigated the potential utility of circulating eCBs as diagnostic biomarkers for AD or the impact of central eCBs on cognition...
  40. pmc A polymorphism in CALHM1 influences Ca2+ homeostasis, Abeta levels, and Alzheimer's disease risk
    Ute Dreses-Werringloer
    Litwin Zucker Research Center for the Study of Alzheimer s Disease, The Feinstein Institute for Medical Research, North Shore LIJ, Manhasset, NY 11030, USA
    Cell 133:1149-61. 2008
    ..We propose that CALHM1 encodes an essential component of a previously uncharacterized cerebral Ca(2+) channel that controls Abeta levels and susceptibility to late-onset AD...
  41. ncbi request reprint Glutathione S-transferase hGSTM3 and ageing-associated neurodegeneration: relationship to Alzheimer's disease
    Tatyana Tchaikovskaya
    Albert Einstein College of Medicine of Yeshiva University, Bronx, NY 10461, USA
    Mech Ageing Dev 126:309-15. 2005
    ..Because hGSTM3 is rich in cysteine residues and readily undergoes S-glutathiolation reactions, deposition of this protein could originate from cross-links produced by oxidative stress...
  42. ncbi request reprint Pin1 colocalization with phosphorylated tau in Alzheimer's disease and other tauopathies
    Pankajavalli Ramakrishnan
    F 526, Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Neurobiol Dis 14:251-64. 2003
    ..Pin1 granules were sparse in PSP, and rarely did A-20 colocalize with TG-3. The appearance of Pin1 granules in the early stages of AD, PiD, and FTDP-17 (P301L) implicates Pin1 in their pathogenesis but not in PSP...
  43. ncbi request reprint Deregulation of cdk5, hyperphosphorylation, and cytoskeletal pathology in the Niemann-Pick type C murine model
    Bitao Bu
    Department of Pathology, University of Washington, Seattle, Washington 98195, USA
    J Neurosci 22:6515-25. 2002
    ..The npc-1 mouse is a valuable in vivo model for determining how and when cdk5 becomes deregulated and whether cdk5 inhibitors would be useful in blocking NPC neurodegeneration...
  44. pmc Amyloid-beta peptide degradation in cell cultures by mycoplasma contaminants
    Haitian Zhao
    Litwin Zucker Research Center for the Study of Alzheimer Disease, The Feinstein Institute for Medical Research, North Shore LIJ, Manhasset, NY, USA
    BMC Res Notes 1:38. 2008
    ..Mycoplasmas are the smallest and simplest self-replicating bacteria and the consequences of an infection for the host cells are variable, ranging from no apparent effect to induction of apoptosis...
  45. pmc Targeting the endocannabinoid system in Alzheimer's disease
    Jeremy Koppel
    The Albert Einstein College of Medicine and The Litwin Zucker Research Center for the Study of Alzheimer s Disease and Memory Disorders, The Feinstein Institute for Medical Research, Manhasset, NY 11030, USA
    J Alzheimers Dis 15:495-504. 2008
    ..Here we present a review of endocannabinoid physiology, the evidence that underscores its utility as a potential target for intervention in Alzheimer's disease, and suggest future pathways of research...
  46. ncbi request reprint Amyloid beta protein precursor is phosphorylated by JNK-1 independent of, yet facilitated by, JNK-interacting protein (JIP)-1
    Meir H Scheinfeld
    Department of Microbiology and Immunology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA
    J Biol Chem 278:42058-63. 2003
    ..Understanding the connection between AbetaPP phosphorylation and the JNK signaling pathway, which mediates cell response to stress may have important implications in understanding the pathogenesis of Alzheimer's disease...
  47. pmc Alpha7 nicotinic acetylcholine receptor: a link between inflammation and neurodegeneration
    Concepcion Conejero-Goldberg
    The Litwin Zucker Research Center for the Study of Alzheimer s Disease, The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, NY 11030, USA
    Neurosci Biobehav Rev 32:693-706. 2008
    ..Among them, alpha7nAChR may represent a pharmacological target to control these two mechanisms during the pathogenesis of neurodegenerative and behavioral disorders...
  48. ncbi request reprint Resveratrol promotes clearance of Alzheimer's disease amyloid-beta peptides
    Philippe Marambaud
    Litwin Zucker Research Center for the Study of Alzheimer s Disease and Memory Disorders, North Shore Long Island Jewish Institute for Medical Research, Manhasset, NY 11030, USA
    J Biol Chem 280:37377-82. 2005
    ..These findings demonstrate a proteasome-dependent anti-amyloidogenic activity of resveratrol and suggest that this natural compound has a therapeutic potential in Alzheimer's disease...
  49. pmc A polymorphic gene nested within an intron of the tau gene: implications for Alzheimer's disease
    Chris Conrad
    Department of Pathology, F526, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA
    Proc Natl Acad Sci U S A 99:7751-6. 2002
    ..The Q7R polymorphism appears to be over-represented in the homozygous state in late onset Alzheimer's disease subjects...