K Iqbal

Summary

Publications

  1. pmc Alzheimer disease therapeutics: focus on the disease and not just plaques and tangles
    Khalid Iqbal
    Department of Neurochemistry, Inge Grundke Iqbal Research Floor, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314, USA Electronic address
    Biochem Pharmacol 88:631-9. 2014
  2. pmc Neurogenic and neurotrophic effects of BDNF peptides in mouse hippocampal primary neuronal cell cultures
    María del Carmen Cárdenas-Aguayo
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York, United States of America
    PLoS ONE 8:e53596. 2013
  3. doi request reprint Microtubule-associated protein tau as a therapeutic target in Alzheimer's disease
    Khalid Iqbal
    New York State Institute for Basic Research in Developmental Disabilities, Department of Neurochemistry, Inge Grundke Iqbal Research Floor, 1050 Forest Hill Road, Staten Island, NY 10314, USA 1 718 494 5259
    Expert Opin Ther Targets 18:307-18. 2014
  4. pmc Mechanisms of tau-induced neurodegeneration
    Khalid Iqbal
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY, 10314, USA
    Acta Neuropathol 118:53-69. 2009
  5. pmc Alzheimer's disease neurofibrillary degeneration: pivotal and multifactorial
    Khalid Iqbal
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York, NY 10314, USA
    Biochem Soc Trans 38:962-6. 2010
  6. pmc Tau in Alzheimer disease and related tauopathies
    K Iqbal
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York 10314 6399, USA
    Curr Alzheimer Res 7:656-64. 2010
  7. pmc Alzheimer's disease, a multifactorial disorder seeking multitherapies
    Khalid Iqbal
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY, USA
    Alzheimers Dement 6:420-4. 2010
  8. doi request reprint Opportunities and challenges in developing Alzheimer disease therapeutics
    Khalid Iqbal
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, 10314 6399, USA
    Acta Neuropathol 122:543-9. 2011
  9. ncbi request reprint Tau is phosphorylated by GSK-3 at several sites found in Alzheimer disease and its biological activity markedly inhibited only after it is prephosphorylated by A-kinase
    J Z Wang
    Chemical Neuropathology Department, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY 10314 6399, USA
    FEBS Lett 436:28-34. 1998
  10. ncbi request reprint Phosphorylation of microtubule-associated protein tau is regulated by protein phosphatase 2A in mammalian brain. Implications for neurofibrillary degeneration in Alzheimer's disease
    C X Gong
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York 10314 6399, USA
    J Biol Chem 275:5535-44. 2000

Research Grants

  1. Subgroups of Alzheimer Disease
    Khalid Iqbal; Fiscal Year: 2010
  2. Subgroups of Alzheimer Disease
    Khalid Iqbal; Fiscal Year: 2007
  3. Abnormal Hyperphosphorylation of Tau
    Khalid Iqbal; Fiscal Year: 2007
  4. Abnormal Hyperphosphorylation of Tau
    Khalid Iqbal; Fiscal Year: 2006
  5. Abnormal Hyperphosphorylation of Tau
    Khalid Iqbal; Fiscal Year: 2005
  6. Abnormal Hyperphosphorylation of Tau
    Khalid Iqbal; Fiscal Year: 2004
  7. Abnormal Hyperphosphorylation of Tau
    Khalid Iqbal; Fiscal Year: 2003
  8. Abnormal Hyperphosphorylation of Tau
    Khalid Iqbal; Fiscal Year: 2009
  9. Abnormal Hyperphosphorylation of Tau
    Khalid Iqbal; Fiscal Year: 2010
  10. Abnormal Hyperphosphorylation of Tau
    Khalid Iqbal; Fiscal Year: 2002

Collaborators

Detail Information

Publications84

  1. pmc Alzheimer disease therapeutics: focus on the disease and not just plaques and tangles
    Khalid Iqbal
    Department of Neurochemistry, Inge Grundke Iqbal Research Floor, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314, USA Electronic address
    Biochem Pharmacol 88:631-9. 2014
    ..Treatment of AD will require both inhibition of neurodegeneration and regeneration of the brain. ..
  2. pmc Neurogenic and neurotrophic effects of BDNF peptides in mouse hippocampal primary neuronal cell cultures
    María del Carmen Cárdenas-Aguayo
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York, United States of America
    PLoS ONE 8:e53596. 2013
    ....
  3. doi request reprint Microtubule-associated protein tau as a therapeutic target in Alzheimer's disease
    Khalid Iqbal
    New York State Institute for Basic Research in Developmental Disabilities, Department of Neurochemistry, Inge Grundke Iqbal Research Floor, 1050 Forest Hill Road, Staten Island, NY 10314, USA 1 718 494 5259
    Expert Opin Ther Targets 18:307-18. 2014
    ..Alzheimer's disease (AD) is a major public health problem in modern society and as yet, other than a few symptomatic drugs, there is no disease-modifying treatment for this disease available...
  4. pmc Mechanisms of tau-induced neurodegeneration
    Khalid Iqbal
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY, 10314, USA
    Acta Neuropathol 118:53-69. 2009
    ..AD is multifactorial and heterogeneous and involves more than one etiopathogenic mechanism...
  5. pmc Alzheimer's disease neurofibrillary degeneration: pivotal and multifactorial
    Khalid Iqbal
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York, NY 10314, USA
    Biochem Soc Trans 38:962-6. 2010
    ..Restoration of PP2A activity by inhibition of the cleavage of I(2)(PP2A)/SET offers a promising therapeutic opportunity in AD with this aetiopathogenic mechanism...
  6. pmc Tau in Alzheimer disease and related tauopathies
    K Iqbal
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York 10314 6399, USA
    Curr Alzheimer Res 7:656-64. 2010
    ..Inhibition of abnormal hyperphosphorylation of tau offers a promising therapeutic target for AD and related tauopathies...
  7. pmc Alzheimer's disease, a multifactorial disorder seeking multitherapies
    Khalid Iqbal
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY, USA
    Alzheimers Dement 6:420-4. 2010
    ..Levels of disease markers in the cerebrospinal fluid are promising, both in identifying various subgroups of AD and in monitoring the response to therapeutic drugs...
  8. doi request reprint Opportunities and challenges in developing Alzheimer disease therapeutics
    Khalid Iqbal
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, 10314 6399, USA
    Acta Neuropathol 122:543-9. 2011
    ..Development of both drugs that can inhibit neurodegeneration and drugs that can increase the regenerative capacity of the brain by enhancing neurogenesis and neuronal plasticity are required to control AD...
  9. ncbi request reprint Tau is phosphorylated by GSK-3 at several sites found in Alzheimer disease and its biological activity markedly inhibited only after it is prephosphorylated by A-kinase
    J Z Wang
    Chemical Neuropathology Department, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY 10314 6399, USA
    FEBS Lett 436:28-34. 1998
    ..Thus a combined role of A-kinase and GSK-3 should be considered in Alzheimer neurofibrillary degeneration...
  10. ncbi request reprint Phosphorylation of microtubule-associated protein tau is regulated by protein phosphatase 2A in mammalian brain. Implications for neurofibrillary degeneration in Alzheimer's disease
    C X Gong
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York 10314 6399, USA
    J Biol Chem 275:5535-44. 2000
    ..A down-regulation of protein phosphatase 2A activity can lead to Alzheimer-like abnormal hyperphosphorylation of tau...
  11. ncbi request reprint Aberrant glycosylation modulates phosphorylation of tau by protein kinase A and dephosphorylation of tau by protein phosphatase 2A and 5
    F Liu
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY 10314, USA
    Neuroscience 115:829-37. 2002
    ..The combined impact of this modulation may be to make tau more susceptible to becoming abnormally hyperphosphorylated...
  12. ncbi request reprint Mechanism of neurofibrillary degeneration and pharmacologic therapeutic approach
    K Iqbal
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island 10314, USA
    J Neural Transm Suppl 59:213-22. 2000
    ..e. PHF/SF. Increase in tau phosphatase activity is a promising approach to inhibit neurofibrillary degeneration and thereby the diseases characterized by this lesion...
  13. pmc Hyperphosphorylation induces self-assembly of tau into tangles of paired helical filaments/straight filaments
    A Alonso
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY 10314, USA
    Proc Natl Acad Sci U S A 98:6923-8. 2001
    ....
  14. ncbi request reprint Post-translational modifications of tau protein in Alzheimer's disease
    C X Gong
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY 10314, USA
    J Neural Transm 112:813-38. 2005
    ..Analyses of the current advances in tau modifications suggest that intervention addressing these abnormalities may offer promising therapeutic opportunities to prevent and treat neurofibrillary degeneration of AD and other tauopathies...
  15. ncbi request reprint Interaction of tau isoforms with Alzheimer's disease abnormally hyperphosphorylated tau and in vitro phosphorylation into the disease-like protein
    A D Alonso
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York 10314, USA
    J Biol Chem 276:37967-73. 2001
    ..Thus, lack of amino-terminal inserts and extra microtubule binding domain repeat in fetal human brain might be protective from Alzheimer's neurofibrillary degeneration...
  16. ncbi request reprint Metabolically active rat brain slices as a model to study the regulation of protein phosphorylation in mammalian brain
    C X Gong
    New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314, USA
    Brain Res Brain Res Protoc 6:134-40. 2001
    ..Furthermore, unlike cultured cells, the neurons in the brain slices reside in the physiological environment of the brain consisting of natural extracellular matrix, neuronal connectivity, and neuronal-glial interactions...
  17. pmc Hyperphosphorylation of microtubule-associated protein tau: a promising therapeutic target for Alzheimer disease
    C X Gong
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York, USA
    Curr Med Chem 15:2321-8. 2008
    ..Development of drugs on the basis of these strategies is likely to lead to disease-modifying therapies for AD...
  18. pmc Alzheimer neurofibrillary degeneration: significance, etiopathogenesis, therapeutics and prevention
    K Iqbal
    Department of Neurochemistry New York State Institute for Basic Research in Developmental Disabilities, Forest Hill Road, Staten Island, New York, NY 10314, USA
    J Cell Mol Med 12:38-55. 2008
    ..The AD subgroup identification of patients can help increase the success of clinical trials and the development of specific and potent disease modifying drugs...
  19. pmc Developing pharmacological therapies for Alzheimer disease
    K Iqbal
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York 10314, USA
    Cell Mol Life Sci 64:2234-44. 2007
    ..Restoration of the phosphatase activity which is downregulated in AD brain or inhibition of GSK-3beta and cdk5, which are required for AD-type abnormal hyperphosphorylation of tau, are among the most promising therapeutic strategies...
  20. ncbi request reprint PP2B isolated from human brain preferentially dephosphorylates Ser-262 and Ser-396 of the Alzheimer disease abnormally hyperphosphorylated tau
    A Rahman
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY, USA
    J Neural Transm 113:219-30. 2006
    ..The preferential dephosphorylation of Ser262 and Ser396 by PP2B suggests a possible involvement of this phosphatase in Alzheimer neurofibrillary degeneration...
  21. ncbi request reprint Multiple forms of phosphatase from human brain: isolation and partial characterization of affi-gel blue nonbinding phosphatase activities
    L Y Cheng
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island 10314, USA
    Neurochem Res 26:425-38. 2001
    ..The resulting dephosphorylated tau regained its activity in promoting the microtubule assembly, suggesting that P7-P11 might regulate the phosphorylation of tau protein in the brain...
  22. ncbi request reprint Tau pathology in Alzheimer disease and other tauopathies
    Khalid Iqbal
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314 6399, USA
    Biochim Biophys Acta 1739:198-210. 2005
    ..Inhibition of this tau abnormality is one of the most promising therapeutic approaches to AD and other tauopathies...
  23. ncbi request reprint Phosphorylation of tau at both Thr 231 and Ser 262 is required for maximal inhibition of its binding to microtubules
    A Sengupta
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island 10314, USA
    Arch Biochem Biophys 357:299-309. 1998
    ..Together, our results indicate that the binding of tau to microtubules is controlled by the phosphorylation of several sites, among which are Thr 231, Ser 235, and Ser 262...
  24. ncbi request reprint Biological markers in Alzheimer's disease
    I Grundke-Iqbal
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York 10314, USA
    Bratisl Lek Listy 107:359-65. 2006
    ..Identification of various subgroups of AD will help improvement in diagnoses and development of potent therapeutic drugs (Tab. 2, Fig. 2, Ref. 53)...
  25. ncbi request reprint Subgroups of Alzheimer's disease based on cerebrospinal fluid molecular markers
    Khalid Iqbal
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY 10314, USA
    Ann Neurol 58:748-57. 2005
    ..These subgroups, which can be identified by CSF analysis, might benefit differently from different therapeutic drugs...
  26. ncbi request reprint Significance and mechanism of Alzheimer neurofibrillary degeneration and therapeutic targets to inhibit this lesion
    Khalid Iqbal
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island 10314 6399, USA
    J Mol Neurosci 19:95-9. 2002
    ....
  27. ncbi request reprint From tangles to tau protein
    K Iqbal
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York, USA
    Bratisl Lek Listy 107:341-2. 2006
    ..Finally, after one hundred years the exact nature of the neurofibrillary tangles and their role in neurodegeneration is beginning to be unraveled...
  28. ncbi request reprint Hyperphosphorylation-induced self assembly of murine tau: a comparison with human tau
    M O Chohan
    Department of Neurochemistry, NYS Institute for Basic Research, Staten Island, NY 10314, USA
    J Neural Transm 112:1035-47. 2005
    ..The filaments obtained from self assembly of murine tau closely resembled those formed from identically treated human tau. Moreover, like human tau, 60-70% of murine tau aggregated on hyperphosphorylation...
  29. ncbi request reprint Inhibition of neurofibrillary degeneration: a promising approach to Alzheimer's disease and other tauopathies
    K Iqbal
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York 10314 6399, USA
    Curr Drug Targets 5:495-502. 2004
    ..Thus, the development of drugs that inhibit neurofibrillary degeneration is a very promising and feasible therapeutic approach to AD and related tauopathies...
  30. pmc Overexpression of Dyrk1A contributes to neurofibrillary degeneration in Down syndrome
    Fei Liu
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Rd, Staten Island, New York 10314, USA
    FASEB J 22:3224-33. 2008
    ..These findings strongly suggest a novel mechanism by which the overexpression of Dyrk1A in DS brain causes neurofibrillary degeneration via hyperphosphorylating tau...
  31. ncbi request reprint Alzheimer neurofibrillary degeneration: therapeutic targets and high-throughput assays
    Khalid Iqbal
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York 10314 6399, USA
    J Mol Neurosci 20:425-9. 2003
    ..Development of high-throughput screening assays for potential drugs aimed at these therapeutic targets is currently under way...
  32. doi request reprint Pharmacologic reversal of neurogenic and neuroplastic abnormalities and cognitive impairments without affecting Aβ and tau pathologies in 3xTg-AD mice
    Julie Blanchard
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, 10314, USA
    Acta Neuropathol 120:605-21. 2010
    ..These findings, for the first time, demonstrate the possibility of therapeutic treatment of AD and related disorders by peripheral administration of a peptide corresponding to a biologically active region of CNTF...
  33. ncbi request reprint Impaired brain glucose metabolism leads to Alzheimer neurofibrillary degeneration through a decrease in tau O-GlcNAcylation
    Cheng Xin Gong
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314 6399, USA
    J Alzheimers Dis 9:1-12. 2006
    ..Further studies of this mechanism are likely to offer a novel therapeutic target for preventing and treating AD...
  34. ncbi request reprint Tau-induced neurodegeneration: a clue to its mechanism
    Alejandra del C Alonso
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York 10314 6399, USA
    J Alzheimers Dis 8:223-6. 2005
  35. pmc Disruption of microtubule network by Alzheimer abnormally hyperphosphorylated tau
    Bin Li
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314 6399, USA
    Acta Neuropathol 113:501-11. 2007
    ..This study, for the first time, provides direct mechanistic insights into the molecular basis of both axonal and dendritic neurodegeneration seen in Alzheimer disease...
  36. ncbi request reprint Memantine inhibits and reverses the Alzheimer type abnormal hyperphosphorylation of tau and associated neurodegeneration
    Liang Li
    Department of Neurochemistry, NYS Institute for Basic Research, 1050 Forest Hill Road, Staten Island, NY 10314 6399, USA
    FEBS Lett 566:261-9. 2004
    ....
  37. pmc Cytosolic abnormally hyperphosphorylated tau but not paired helical filaments sequester normal MAPs and inhibit microtubule assembly
    Khalid Iqbal
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY 10314 6399, USA
    J Alzheimers Dis 14:365-70. 2008
    ..These findings suggest the inhibition of tau abnormal hyperphosphorylation and not the aggregation of tau as the preferred therapeutic target for AD and related tauopathies...
  38. pmc Dysregulation of insulin signaling, glucose transporters, O-GlcNAcylation, and phosphorylation of tau and neurofilaments in the brain: Implication for Alzheimer's disease
    Yanqiu Deng
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York, NY 10314, USA
    Am J Pathol 175:2089-98. 2009
    ....
  39. ncbi request reprint Discoveries of tau, abnormally hyperphosphorylated tau and others of neurofibrillary degeneration: a personal historical perspective
    Khalid Iqbal
    New York State Institute for Basic Research, in Developmental Disabilities, Department of Neurochemistry, 1050 Forest Hill Road, Staten Island, New York 10314 6399, USA
    J Alzheimers Dis 9:219-42. 2006
    ....
  40. pmc Decrease of protein phosphatase 2A and its association with accumulation and hyperphosphorylation of tau in Down syndrome
    Zhihou Liang
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York 10314 6399, USA
    J Alzheimers Dis 13:295-302. 2008
    ..Our results indicate that PP2A is down-regulated in DS brain and suggest that this down-regulation might be involved in the abnormal hyperphosphorylation and accumulation of tau...
  41. pmc Reduced O-GlcNAcylation links lower brain glucose metabolism and tau pathology in Alzheimer's disease
    Fei Liu
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York 10314, USA
    Brain 132:1820-32. 2009
    ..Thus, restoration of brain tau O-GlcNAcylation and protein phosphatase 2A activity may offer promising therapeutic targets for treating Alzheimer's disease...
  42. ncbi request reprint Regulation of phosphorylation of tau by protein kinases in rat brain
    Amitabha Sengupta
    Department of Neurochemistry, New York State Institute for Basic Research, Staten Island, NY 10314 6399, USA
    Neurochem Res 31:1473-80. 2006
    ....
  43. pmc Polymerization of hyperphosphorylated tau into filaments eliminates its inhibitory activity
    Alejandra del C Alonso
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314 6399, USA
    Proc Natl Acad Sci U S A 103:8864-9. 2006
    ....
  44. ncbi request reprint Promotion of hyperphosphorylation by frontotemporal dementia tau mutations
    Alejandra del C Alonso
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York, NY 10314 6399, USA
    J Biol Chem 279:34873-81. 2004
    ..These findings taken together suggest that the mutations in tau might cause neurodegeneration by making the protein a more favorable substrate for hyperphosphorylation...
  45. ncbi request reprint Pharmacological approaches of neurofibrillary degeneration
    Khalid Iqbal
    NYS Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York, 10314 USA att net
    Curr Alzheimer Res 2:335-41. 2005
    ..The development of drugs that inhibit neurofibrillary degeneration is a very promising and feasible therapeutic approach to inhibit the progression of AD and related tauopathies...
  46. ncbi request reprint Role of glycosylation in hyperphosphorylation of tau in Alzheimer's disease
    Fei Liu
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY 10314, USA
    FEBS Lett 512:101-6. 2002
    ..These results suggest that the glycosylation of tau is an early abnormality that can facilitate the subsequent abnormal hyperphosphorylation of tau in AD brain...
  47. ncbi request reprint Neurofibrillary pathology leads to synaptic loss and not the other way around in Alzheimer disease
    Khalid Iqbal
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314 6399, USA
    J Alzheimers Dis 4:235-8. 2002
  48. pmc Anesthesia induces phosphorylation of tau
    Xiaoqin Run
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY 10314 6399, USA
    J Alzheimers Dis 16:619-26. 2009
    ..Our findings also provide a possible mechanism by which anesthesia may cause postoperative cognitive impairment and increase the risk for AD...
  49. pmc O-GlcNAcylation regulates phosphorylation of tau: a mechanism involved in Alzheimer's disease
    Fei Liu
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314, USA
    Proc Natl Acad Sci U S A 101:10804-9. 2004
    ....
  50. ncbi request reprint Phosphothreonine-212 of Alzheimer abnormally hyperphosphorylated tau is a preferred substrate of protein phosphatase-1
    Abdur Rahman
    Department of Neurochemistry, New York Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314, USA
    Neurochem Res 30:277-87. 2005
    ..Of the sites dephosphorylated, pT212 was only a substrate for PP1, as purified/enriched PP2A and PP2B from the same brains did not dephosphorylate this site...
  51. pmc The carboxy-terminal fragment of inhibitor-2 of protein phosphatase-2A induces Alzheimer disease pathology and cognitive impairment
    Xiaochuan Wang
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY 10314, USA
    FASEB J 24:4420-32. 2010
    ..These findings suggest a novel etiopathogenic mechanism of AD, which is initiated by the cleavage of I(2)(PP2A), producing I(2CTF), and describe a novel disease-relevant nontransgenic animal model of AD...
  52. ncbi request reprint Inhibitors of protein phosphatase-2A from human brain structures, immunocytological localization and activities towards dephosphorylation of the Alzheimer type hyperphosphorylated tau
    Ichiro Tsujio
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314 6399, USA
    FEBS Lett 579:363-72. 2005
    ..Overexpression of I(1)(PP2A) as well as I(2)(PP2A) results in tau hyperphosphorylation and degeneration of PC 12 cells...
  53. pmc Brain glucose transporters, O-GlcNAcylation and phosphorylation of tau in diabetes and Alzheimer's disease
    Ying Liu
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York, USA
    J Neurochem 111:242-9. 2009
    ..These results suggest that T2DM may contribute to the increased risk for AD by impairing brain glucose uptake/metabolism and, consequently, down-regulation of O-GlcNAcylation, which facilitates abnormal hyperphosphorylation of tau...
  54. pmc Regulation between O-GlcNAcylation and phosphorylation of neurofilament-M and their dysregulation in Alzheimer disease
    Yanqiu Deng
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Rd, Staten Island, NY 10314, USA
    FASEB J 22:138-45. 2008
    ....
  55. pmc Developmental regulation of tau phosphorylation, tau kinases, and tau phosphatases
    Yang Yu
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York, USA
    J Neurochem 108:1480-94. 2009
    ..These studies provide new insight into the developmental regulation of site-specific tau phosphorylation and identify the likely sites required for the abnormal hyperphosphorylation of tau in AD...
  56. ncbi request reprint Mechanism of tau-induced neurodegeneration in Alzheimer disease and related tauopathies
    Alejandra del C Alonso
    Department of Biology and Center for Developmental Neuroscience and Developmental Disabilities, College of Staten Island, The City University of New York, Staten Island, NY 10314, USA
    Curr Alzheimer Res 5:375-84. 2008
    ..Finally, we consider whether tau accumulation or its conformational change is related to tau-induced neurodegeneration, and we propose a mechanism of neurodegeneration...
  57. pmc Decreased glucose transporters correlate to abnormal hyperphosphorylation of tau in Alzheimer disease
    Ying Liu
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314, USA
    FEBS Lett 582:359-64. 2008
    ....
  58. pmc Regulation of phosphorylation of tau by cyclin-dependent kinase 5 and glycogen synthase kinase-3 at substrate level
    Amitabha Sengupta
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York 10314 6399, USA
    FEBS Lett 580:5925-33. 2006
    ..These findings suggest that the phosphorylation of tau at Thr231 and Ser262 by cdk5 plus GSK-3, which inhibits its normal biological activity, is regulated both by its amino terminal inserts and its physical state...
  59. ncbi request reprint Dephosphorylation of microtubule-associated protein tau by protein phosphatase 5
    Cheng Xin Gong
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York 10314, USA
    J Neurochem 88:298-310. 2004
    ..These results suggest that PP5 plays a role in the dephosphorylation of tau and might be involved in the molecular pathogenesis of Alzheimer's disease...
  60. ncbi request reprint Contributions of protein phosphatases PP1, PP2A, PP2B and PP5 to the regulation of tau phosphorylation
    Fei Liu
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York 10314, USA
    Eur J Neurosci 22:1942-50. 2005
    ..Our findings indicate that PP2A is the major tau phosphatase that regulates its phosphorylation at multiple sites in human brain. The abnormal hyperphosphorylation of tau is partially due to a downregulation of PP2A activity in AD brain...
  61. ncbi request reprint Involvement of aberrant glycosylation in phosphorylation of tau by cdk5 and GSK-3beta
    Fei Liu
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island 10314, USA
    FEBS Lett 530:209-14. 2002
    ..These data suggest that aberrant glycosylation of tau in AD might be involved in neurofibrillary degeneration by promoting abnormal hyperphosphorylation by cdk5 and GSK-3beta...
  62. ncbi request reprint The dentate gyrus neurogenesis: a therapeutic target for Alzheimer's disease
    Yoshitaka Tatebayashi
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York 10314, USA
    Acta Neuropathol 105:225-32. 2003
    ....
  63. pmc Site-specific effects of tau phosphorylation on its microtubule assembly activity and self-aggregation
    Fei Liu
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314, USA
    Eur J Neurosci 26:3429-36. 2007
    ..These studies reveal the differential regulation of tau's biological activity and self-aggregation by phosphorylation at various sites/regions...
  64. ncbi request reprint Dephosphorylation of tau by protein phosphatase 5: impairment in Alzheimer's disease
    Fei Liu
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York 10314, USA
    J Biol Chem 280:1790-6. 2005
    ..These results suggest that tau is probably a physiological substrate of PP5 and that the abnormal hyperphosphorylation of tau in AD might result in part from the decreased PP5 activity in the diseased brains...
  65. ncbi request reprint From tau to toxicity: emerging roles of NMDA receptor in Alzheimer's disease
    Muhammad Omar Chohan
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York 10314 6399, USA
    J Alzheimers Dis 10:81-7. 2006
    ..Here, we analyze some of the most intriguing evidence for NMDA receptor-mediated cellular dysfunction and propose a mechanism by which hyperactive NMDA receptors might lead to neurofibrillary degeneration in Alzheimer's disease...
  66. ncbi request reprint Regulation of microtubule-associated proteins, protein kinases and protein phosphatases during differentiation of SY5Y cells
    Niloufar Haque
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314 6399, USA
    Brain Res Mol Brain Res 129:163-70. 2004
    ..These results suggest that the expression, post-translational modifications and biological activities of various MAPs are differentially regulated to meet the biological needs during cell differentiation...
  67. ncbi request reprint Role of tau phosphorylation by glycogen synthase kinase-3beta in the regulation of organelle transport
    Yoshitaka Tatebayashi
    New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York, NY 10314, USA
    J Cell Sci 117:1653-63. 2004
    ..These findings raise the possibility that the phosphorylation of tau by glycogen synthase kinase-3 might be involved in the regulation of organelle transport...
  68. ncbi request reprint Targeting tau protein in Alzheimer's disease
    Cheng Xin Gong
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314, USA
    Drugs Aging 27:351-65. 2010
    ....
  69. pmc PKA modulates GSK-3beta- and cdk5-catalyzed phosphorylation of tau in site- and kinase-specific manners
    Fei Liu
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314, USA
    FEBS Lett 580:6269-74. 2006
    ..These studies reveal the nature of the inter-regulation of tau phosphorylation by the three major tau kinases...
  70. ncbi request reprint Involvement of I2PP2A in the abnormal hyperphosphorylation of tau and its reversal by Memantine
    Muhammad Omar Chohan
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314 6399, USA
    FEBS Lett 580:3973-9. 2006
    ..These findings demonstrate novel mechanisms by which I2PP2A regulates the intracellular activity of PP2A and phosphorylation of tau, and by which Memantine modulates PP2A signaling and inhibits neurofibrillary degeneration...
  71. pmc Tau in cerebrospinal fluid: a sensitive sandwich enzyme-linked immunosorbent assay using tyramide signal amplification
    Hidenaga Yamamori
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY, USA
    Neurosci Lett 418:186-9. 2007
    ..A highly significant correlation was found between this assay and a commonly used kit, INNOTEST hTAU Antigen...
  72. pmc Up-regulation of inhibitors of protein phosphatase-2A in Alzheimer's disease
    Hitoshi Tanimukai
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York 10314 6399, USA
    Am J Pathol 166:1761-71. 2005
    ..These studies suggest the possible involvement of I1(PP2A) and I2(PP2A) in the abnormal hyperphosphorylation of tau in AD...
  73. pmc Down-regulation of cAMP-dependent protein kinase by over-activated calpain in Alzheimer disease brain
    Zhihou Liang
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York, USA
    J Neurochem 103:2462-70. 2007
    ....
  74. pmc Failure of neuronal maturation in Alzheimer disease dentate gyrus
    Bin Li
    Department of Neurochemistry, NYS Institute for Basic Research in Developmental Disabilities, Staten Island, New York 10314, USA
    J Neuropathol Exp Neurol 67:78-84. 2008
    ..These findings suggest that newly generated neurons in Alzheimer disease dentate gyrus do not become mature neurons, although neuroproliferation is increased...
  75. pmc I1PP2A affects tau phosphorylation via association with the catalytic subunit of protein phosphatase 2A
    She Chen
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York 10314, USA
    J Biol Chem 283:10513-21. 2008
    ..Double immunofluorescence staining showed that I (1)(PP2A) and I (1)(PP2A)DeltaC2 increased Tau phosphorylation and impaired the microtubule network and neurite outgrowth in PC12 cells treated with nerve growth factor...
  76. ncbi request reprint Metabolic/signal transduction hypothesis of Alzheimer's disease and other tauopathies
    Khalid Iqbal
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, 10314 6399, USA
    Acta Neuropathol 109:25-31. 2005
    ..The hyperphosphorylated tau sequesters normal tau, MAP1 and MAP2, which results in breakdown of the microtubule network and, consequently, a progressive retrograde degeneration of the affected neurons and, ultimately, dementia...
  77. pmc Dysregulation of tau phosphorylation in mouse brain during excitotoxic damage
    Zhihou Liang
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY 10314 6399, USA
    J Alzheimers Dis 17:531-9. 2009
    ....
  78. pmc Cerebrospinal fluid secretory Ca2+-dependent phospholipase A2 activity is increased in Alzheimer disease
    Sonia Chalbot
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York 10314 6399, USA
    Clin Chem 55:2171-9. 2009
    ....
  79. ncbi request reprint Inhibition of protein phosphatase 2A induces phosphorylation and accumulation of neurofilaments in metabolically active rat brain slices
    Cheng Xin Gong
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York, NY 10314, USA
    Neurosci Lett 340:107-10. 2003
    ..These findings suggest that the hyperphosphorylation and accumulation of NF found in AD brain could have been caused by the down-regulation of PP2A...
  80. ncbi request reprint Truncation and activation of calcineurin A by calpain I in Alzheimer disease brain
    Fei Liu
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, 10314, USA
    J Biol Chem 280:37755-62. 2005
    ..These findings suggest that the overactivation of calpain I and calcineurin may mediate the role of calcium homeostatic disturbance in the neurodegeneration of AD...
  81. pmc Stratification of patients is the way to go to develop neuroprotective/disease-modifying drugs for Alzheimer's disease
    Khalid Iqbal
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York, NY 10314, USA att net
    J Alzheimers Dis 15:339-45. 2008
    ..The employment of these subgroups of AD in clinical trials can markedly increase the success in developing specific and potent therapeutic drugs...
  82. ncbi request reprint NF-kappaB precursor, p105, and NF-kappaB inhibitor, IkappaBgamma, are both elevated in Alzheimer disease brain
    Yu Huang
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314 6399, USA
    Neurosci Lett 373:115-8. 2005
    ..Our findings suggest that the NF-kappaB pathway might be involved in the molecular mechanism of AD...
  83. ncbi request reprint Elevation of the level and activity of acid ceramidase in Alzheimer's disease brain
    Yu Huang
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York 10314 6399, USA
    Eur J Neurosci 20:3489-97. 2004
    ..Our findings suggest that AC might play a role in controlling neuronal apoptosis and that AC-mediated signalling pathways might be involved in the molecular mechanism of AD...

Research Grants13

  1. Subgroups of Alzheimer Disease
    Khalid Iqbal; Fiscal Year: 2010
    ....
  2. Subgroups of Alzheimer Disease
    Khalid Iqbal; Fiscal Year: 2007
    ....
  3. Abnormal Hyperphosphorylation of Tau
    Khalid Iqbal; Fiscal Year: 2007
    ..The studies will lead also to the generation of a cellular and an animal model of tauopathies, which can be used for the development of therapeutic drugs for diseases characterized by this lesion. ..
  4. Abnormal Hyperphosphorylation of Tau
    Khalid Iqbal; Fiscal Year: 2006
    ..These studies will help elucidate the role of PP-2A- and PP-1- inhibitors in the abnormal hyperphosphorylation of tau and the neurodegeneration that occurs in AD. ..
  5. Abnormal Hyperphosphorylation of Tau
    Khalid Iqbal; Fiscal Year: 2005
    ..These studies will help elucidate the role of PP-2A- and PP-1- inhibitors in the abnormal hyperphosphorylation of tau and the neurodegeneration that occurs in AD. ..
  6. Abnormal Hyperphosphorylation of Tau
    Khalid Iqbal; Fiscal Year: 2004
    ..These studies will help elucidate the role of PP-2A- and PP-1- inhibitors in the abnormal hyperphosphorylation of tau and the neurodegeneration that occurs in AD. ..
  7. Abnormal Hyperphosphorylation of Tau
    Khalid Iqbal; Fiscal Year: 2003
    ..These studies will help elucidate the role of PP-2A- and PP-1- inhibitors in the abnormal hyperphosphorylation of tau and the neurodegeneration that occurs in AD. ..
  8. Abnormal Hyperphosphorylation of Tau
    Khalid Iqbal; Fiscal Year: 2009
    ..The studies will lead also to the generation of a cellular and an animal model of tauopathies, which can be used for the development of therapeutic drugs for diseases characterized by this lesion. ..
  9. Abnormal Hyperphosphorylation of Tau
    Khalid Iqbal; Fiscal Year: 2010
    ..The studies will lead also to the generation of a cellular and an animal model of tauopathies, which can be used for the development of therapeutic drugs for diseases characterized by this lesion. ..
  10. Abnormal Hyperphosphorylation of Tau
    Khalid Iqbal; Fiscal Year: 2002
    ..These studies will help elucidate the role of PP-2A- and PP-1- inhibitors in the abnormal hyperphosphorylation of tau and the neurodegeneration that occurs in AD. ..
  11. Subgroups of Alzheimer Disease
    Khalid Iqbal; Fiscal Year: 2009
    ....