Changiz Geula

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. ncbi request reprint The 2nd International Symposium on Alzheimer's disease and related disorders in the Middle East, May 1-3, 2003, Istanbul, Turkey
    Changiz Geula
    Laboratory for Neurodegenerative and Aging Research, Department of Medicine, Harvard Medical School, Boston, MA 02215, USA
    Amyloid 11:276-80. 2004
  2. ncbi request reprint Loss of calbindin-D28K from aging human cholinergic basal forebrain: relation to plaques and tangles
    Changiz Geula
    Laboratory for Neurodegenerative and Aging Research, Section of Gerontology, Beth Israel Deaconess Medical Center, Department of Medicine, Harvard Medical School, Boston, Massachusetts 02215, USA
    J Neuropathol Exp Neurol 62:605-16. 2003
  3. ncbi request reprint Butyrylcholinesterase, cholinergic neurotransmission and the pathology of Alzheimer's disease
    Changiz Geula
    Laboratory for Neurodegenerative and Aging Research, Department of Medicine Neuroscience, Harvard Medical School and Division of Gerontology, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA
    Drugs Today (Barc) 40:711-21. 2004
  4. ncbi request reprint DJ-1 transcriptionally up-regulates the human tyrosine hydroxylase by inhibiting the sumoylation of pyrimidine tract-binding protein-associated splicing factor
    Nan Zhong
    Department of Neurology, Caritas St Elizabeth s Medical Center, Tufts University School of Medicine, Boston, Massachusetts 02135, USA
    J Biol Chem 281:20940-8. 2006
  5. ncbi request reprint Distribution, progression and chemical composition of cortical amyloid-beta deposits in aged rhesus monkeys: similarities to the human
    Sepehr Sani
    Laboratory for Neurodegenerative and Aging Research, Department of Medicine Neuroscience, Harvard Medical School and Section of Gerontology, Beth Israel Deaconess Medical Center, 21 27 Burlington Ave, Boston, MA 02215, USA
    Acta Neuropathol 105:145-56. 2003
  6. ncbi request reprint Ccr2 deficiency impairs microglial accumulation and accelerates progression of Alzheimer-like disease
    Joseph El Khoury
    Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, 149 13th Street, Charlestown, Massachusetts 02129, USA
    Nat Med 13:432-8. 2007
  7. ncbi request reprint Loss of calbindin-D28k from aging human cholinergic basal forebrain: relation to neuronal loss
    Changiz Geula
    Laboratory for Neurodegenerative and Aging Research, Section of Gerontology, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA
    J Comp Neurol 455:249-59. 2003
  8. ncbi request reprint Calbindin-D28K, parvalbumin and calretinin in primate lower motor neurons
    Ashkan Fahandejsaadi
    Laboratory for Neurodegenerative and Aging Research, Department of Medicine, Harvard Medical School and Section of Gerontology, Beth Israel Deaconess Medical Center, 330 Brookline Ave, Burlington Research Building, Boston, MA 02215, USA
    Neuroreport 15:443-8. 2004
  9. ncbi request reprint Rivastigmine is a potent inhibitor of acetyl- and butyrylcholinesterase in Alzheimer's plaques and tangles
    Mariam F Eskander
    Laboratory for Neurodegenerative and Aging Research, Department of Medicine Neuroscience, Harvard Medical School and Division of Gerontology, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA
    Brain Res 1060:144-52. 2005
  10. ncbi request reprint Amyloid-beta deposits in the cerebral cortex of the aged common marmoset (Callithrix jacchus): incidence and chemical composition
    Changiz Geula
    Department of Medicine, Harvard Medical School and Beth Israel Deaconess Medical Center, Boston, MA 02215, USA
    Acta Neuropathol 103:48-58. 2002

Collaborators

Detail Information

Publications21

  1. ncbi request reprint The 2nd International Symposium on Alzheimer's disease and related disorders in the Middle East, May 1-3, 2003, Istanbul, Turkey
    Changiz Geula
    Laboratory for Neurodegenerative and Aging Research, Department of Medicine, Harvard Medical School, Boston, MA 02215, USA
    Amyloid 11:276-80. 2004
  2. ncbi request reprint Loss of calbindin-D28K from aging human cholinergic basal forebrain: relation to plaques and tangles
    Changiz Geula
    Laboratory for Neurodegenerative and Aging Research, Section of Gerontology, Beth Israel Deaconess Medical Center, Department of Medicine, Harvard Medical School, Boston, Massachusetts 02215, USA
    J Neuropathol Exp Neurol 62:605-16. 2003
    ..It is likely that loss of CB from the BFCN and formation of plaques and tangles are part of general age-related processes that occur in parallel rather than being causally related...
  3. ncbi request reprint Butyrylcholinesterase, cholinergic neurotransmission and the pathology of Alzheimer's disease
    Changiz Geula
    Laboratory for Neurodegenerative and Aging Research, Department of Medicine Neuroscience, Harvard Medical School and Division of Gerontology, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA
    Drugs Today (Barc) 40:711-21. 2004
    ..Therefore, inhibition of butyrylcholinesterase will not only lead to enhanced cholinergic transmission but also has the potential to interfere with the disease process in Alzheimer's disease and other dementing disorders...
  4. ncbi request reprint DJ-1 transcriptionally up-regulates the human tyrosine hydroxylase by inhibiting the sumoylation of pyrimidine tract-binding protein-associated splicing factor
    Nan Zhong
    Department of Neurology, Caritas St Elizabeth s Medical Center, Tufts University School of Medicine, Boston, Massachusetts 02135, USA
    J Biol Chem 281:20940-8. 2006
    ..Therefore, our results suggest DJ-1 as a regulator of protein sumoylation and directly link the loss of DJ-1 expression and transcriptional dysfunction to impaired dopamine synthesis...
  5. ncbi request reprint Distribution, progression and chemical composition of cortical amyloid-beta deposits in aged rhesus monkeys: similarities to the human
    Sepehr Sani
    Laboratory for Neurodegenerative and Aging Research, Department of Medicine Neuroscience, Harvard Medical School and Section of Gerontology, Beth Israel Deaconess Medical Center, 21 27 Burlington Ave, Boston, MA 02215, USA
    Acta Neuropathol 105:145-56. 2003
    ..Therefore, despite some differences from the human, the aged rhesus may be a good model for studies of the pathological effects of Abeta in the primate brain...
  6. ncbi request reprint Ccr2 deficiency impairs microglial accumulation and accelerates progression of Alzheimer-like disease
    Joseph El Khoury
    Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, 149 13th Street, Charlestown, Massachusetts 02129, USA
    Nat Med 13:432-8. 2007
    ..Thus, Ccr2-dependent microglial accumulation plays a protective role in the early stages of Alzheimer disease by promoting Abeta clearance...
  7. ncbi request reprint Loss of calbindin-D28k from aging human cholinergic basal forebrain: relation to neuronal loss
    Changiz Geula
    Laboratory for Neurodegenerative and Aging Research, Section of Gerontology, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA
    J Comp Neurol 455:249-59. 2003
    ....
  8. ncbi request reprint Calbindin-D28K, parvalbumin and calretinin in primate lower motor neurons
    Ashkan Fahandejsaadi
    Laboratory for Neurodegenerative and Aging Research, Department of Medicine, Harvard Medical School and Section of Gerontology, Beth Israel Deaconess Medical Center, 330 Brookline Ave, Burlington Research Building, Boston, MA 02215, USA
    Neuroreport 15:443-8. 2004
    ..CBP immunoreactivity within motor neurons was of variable staining intensity. It remains to be established whether the presence of these CBPs confers protection against the pathogenic mechanisms of motor neuron disease...
  9. ncbi request reprint Rivastigmine is a potent inhibitor of acetyl- and butyrylcholinesterase in Alzheimer's plaques and tangles
    Mariam F Eskander
    Laboratory for Neurodegenerative and Aging Research, Department of Medicine Neuroscience, Harvard Medical School and Division of Gerontology, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA
    Brain Res 1060:144-52. 2005
    ..Thus, at the therapeutic concentrations used, rivastigmine is likely to result in inhibition of pathological cholinesterases, with the potential of interfering with the disease process...
  10. ncbi request reprint Amyloid-beta deposits in the cerebral cortex of the aged common marmoset (Callithrix jacchus): incidence and chemical composition
    Changiz Geula
    Department of Medicine, Harvard Medical School and Beth Israel Deaconess Medical Center, Boston, MA 02215, USA
    Acta Neuropathol 103:48-58. 2002
    ..However, the relatively small number of animals which can be expected to reach old age severely limits the utility of this species as a model of A beta deposition...
  11. ncbi request reprint Comparative distribution of tau phosphorylated at Ser262 in pre-tangles and tangles
    Jane Lauckner
    Laboratory for Neurodegenerative and Aging Research, Department of Medicine, Harvard Medical School, Boston, MA 02215, USA
    Neurobiol Aging 24:767-76. 2003
    ....
  12. ncbi request reprint Age-related changes in calbindin-D28k, calretinin, and parvalbumin-immunoreactive neurons in the human cerebral cortex
    Jing Bu
    Laboratory for Neurodegenerative and Aging Research, Harvard Medical School, and Section of Gerontology, Beth Israel Deaconess Medical Center, 330 Brookline Ave, Burlington Research Facility, Boston, MA 02215, USA
    Exp Neurol 182:220-31. 2003
    ....
  13. ncbi request reprint Butyrylcholinesterase activity in the rat forebrain and upper brainstem: postnatal development and adult distribution
    Changiz Geula
    Laboratory for Neurodegenerative and Aging Research, Harvard Medical School, and Division of Gerontology, Beth Israel Deaconess Medical Center, Boston, MA, USA
    Exp Neurol 204:640-57. 2007
    ..The transient presence of BuChE activity of very low intensity in all neurons and of higher intensity in thalamic neurons supports the implied role for this enzyme in neuronal development...
  14. ncbi request reprint Mitochondrial DNA deletions are abundant and cause functional impairment in aged human substantia nigra neurons
    Yevgenya Kraytsberg
    Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA
    Nat Genet 38:518-20. 2006
    ..The fraction of mtDNA deletions is significantly higher in cytochrome c oxidase (COX)-deficient neurons than in COX-positive neurons, suggesting that mtDNA deletions may be directly responsible for impaired cellular respiration...
  15. ncbi request reprint The Parkinson's disease-associated DJ-1 protein is a transcriptional co-activator that protects against neuronal apoptosis
    Jin Xu
    Department of Neurology, Caritas St Elizabeth s Center, Tufts University School of Medicine, Boston, MA 02135, USA
    Hum Mol Genet 14:1231-41. 2005
    ..Mutations that impair the transcriptional co-activator function of DJ-1 render dopaminergic neurons vulnerable to apoptosis and may contribute to the pathogenesis of PD...
  16. ncbi request reprint A CD36-initiated signaling cascade mediates inflammatory effects of beta-amyloid
    Kathryn J Moore
    Lipid Metabolism Unit, Massachusetts General Hospital, Harvard Medical School, Boston 02114, USA
    J Biol Chem 277:47373-9. 2002
    ....
  17. pmc Cholinergic neuronal and axonal abnormalities are present early in aging and in Alzheimer disease
    Changiz Geula
    Laboratory for Cognitive and Molecular Morphometry, Cognitive Neurology and Alzheimer s Disease Center, Northwestern University Medical School, Chicago, Illinois 60611, USA
    J Neuropathol Exp Neurol 67:309-18. 2008
    ..Therefore, despite the morphologic alterations, choline acetyltransferase activity, but not necessarily normal neuron functions, may be preserved...
  18. ncbi request reprint Apoptotic signals within the basal forebrain cholinergic neurons in Alzheimer's disease
    Chuang Kuo Wu
    Alzheimer Disease and Memory Disorders Center, Department of Neurology, Memorial Hospital of Rhode Island, 111, Brewster Street, Pawtucket, RI 02860, USA
    Exp Neurol 195:484-96. 2005
    ..The findings also suggest possible relationships between loss of CB, FADD expression and phosphorylation of tau within the basal forebrain cholinergic neurons in AD...
  19. ncbi request reprint Tomographic visualization of cholinesterase
    Rodrigo O Kuljis
    Ann Neurol 60:745-6. 2006
  20. ncbi request reprint The 3rd International Symposium on Alzheimer's Disease and Related Disorders in the Middle East, Istanbul, Turkey, October 1 - 2, 2005
    Robert P Friedland
    Department of Neurology, Case School of Medicine, Cleveland, OH 44106, USA
    Amyloid 14:161-8. 2007
  21. ncbi request reprint Neurobiology of butyrylcholinesterase
    Sultan Darvesh
    Department of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada
    Nat Rev Neurosci 4:131-8. 2003