ELLIOTT JAY MUFSON

Summary

Affiliation: Rush University Medical Center
Country: USA

Publications

  1. ncbi request reprint The role of nerve growth factor receptors in cholinergic basal forebrain degeneration in prodromal Alzheimer disease
    Scott E Counts
    Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois 60612, USA
    J Neuropathol Exp Neurol 64:263-72. 2005
  2. ncbi request reprint A phase 1 clinical trial of nerve growth factor gene therapy for Alzheimer disease
    Mark H Tuszynski
    Department of Neurosciences, University of California at San Diego, La Jolla 92093, USA
    Nat Med 11:551-5. 2005
  3. ncbi request reprint Cognitive performance correlates with cortical isopeptide immunoreactivity as well as Alzheimer type pathology
    Deng Shun Wang
    Departments of Neuroscience and Pathology, Mayo Clinic College of Medicine, 4500 San Pablo Road, Jacksonville, FL 32224, USA
    J Alzheimers Dis 13:53-66. 2008
  4. ncbi request reprint Preservation of brain nerve growth factor in mild cognitive impairment and Alzheimer disease
    Elliott J Mufson
    Department of Neurological Sciences, Rush Presbyterian St Luke s Medical Center, 2242 W Harrison Street, Chicago, IL 60612, USA
    Arch Neurol 60:1143-8. 2003
  5. pmc Hippocampal proNGF signaling pathways and β-amyloid levels in mild cognitive impairment and Alzheimer disease
    Elliott J Mufson
    Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA
    J Neuropathol Exp Neurol 71:1018-29. 2012
  6. ncbi request reprint m2 muscarinic acetylcholine receptor-immunoreactive neurons are not reduced within the nucleus basalis in Alzheimer's disease: relationship with cholinergic and galaninergic perikarya
    E J Mufson
    Department of Neurological Sciences, Rush Presbyterian St Luke s Medical Center, Chicago, Illinois 60612, USA
    J Comp Neurol 392:313-29. 1998
  7. pmc Preservation of cortical sortilin protein levels in MCI and Alzheimer's disease
    Elliott J Mufson
    Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA
    Neurosci Lett 471:129-33. 2010
  8. pmc Cholinergic system during the progression of Alzheimer's disease: therapeutic implications
    Elliott J Mufson
    Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA
    Expert Rev Neurother 8:1703-18. 2008
  9. ncbi request reprint Nerve growth factor: structure, function and therapeutic implications for Alzheimer's disease
    Shivanand P Lad
    Department of Neurological Sciences and Rush Alzheimer s Disease Center, Rush Presbyterian St Luke s Medical School, Chicago, IL 60612, USA
    Curr Drug Targets CNS Neurol Disord 2:315-34. 2003
  10. ncbi request reprint Human cholinergic basal forebrain: chemoanatomy and neurologic dysfunction
    Elliott J Mufson
    Department of Neurological Sciences and Alzheimer s Disease Center, Rush Presbyterian St Luke s Medical Center, Tech 2000, 2242 West Harrison St, Suite 200, Chicago, IL 60612, USA
    J Chem Neuroanat 26:233-42. 2003

Research Grants

  1. GALANIN IN ALZHEIMER'S DISEASE
    Elliott Mufson; Fiscal Year: 2007
  2. TRAINING IN AGE-RELATED NEURODEGENERATIVE DISEASES
    Elliott Mufson; Fiscal Year: 2007
  3. GALANIN IN ALZHEIMER'S DISEASE
    Elliott Mufson; Fiscal Year: 2009
  4. GALANIN IN ALZHEIMER'S DISEASE
    Elliott Mufson; Fiscal Year: 1999
  5. GALANIN IN ALZHEIMER'S DISEASE
    Elliott Mufson; Fiscal Year: 1991
  6. GALANIN IN ALZHEIMER'S DISEASE
    Elliott Mufson; Fiscal Year: 1992
  7. GALANIN IN ALZHEIMER'S DISEASE
    Elliott Mufson; Fiscal Year: 1993
  8. Galanin in Alzheimer's Disease
    ELLIOTT JAY MUFSON; Fiscal Year: 2010

Detail Information

Publications70

  1. ncbi request reprint The role of nerve growth factor receptors in cholinergic basal forebrain degeneration in prodromal Alzheimer disease
    Scott E Counts
    Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois 60612, USA
    J Neuropathol Exp Neurol 64:263-72. 2005
    ..Therapeutic neurotrophic intervention might delay or prevent NB neuron degeneration and preserve cholinergic cortical function during prodromal AD...
  2. ncbi request reprint A phase 1 clinical trial of nerve growth factor gene therapy for Alzheimer disease
    Mark H Tuszynski
    Department of Neurosciences, University of California at San Diego, La Jolla 92093, USA
    Nat Med 11:551-5. 2005
    ..05) increases in cortical 18-fluorodeoxyglucose after treatment. Brain autopsy from one subject suggested robust growth responses to NGF. Additional clinical trials of NGF for Alzheimer disease are warranted...
  3. ncbi request reprint Cognitive performance correlates with cortical isopeptide immunoreactivity as well as Alzheimer type pathology
    Deng Shun Wang
    Departments of Neuroscience and Pathology, Mayo Clinic College of Medicine, 4500 San Pablo Road, Jacksonville, FL 32224, USA
    J Alzheimers Dis 13:53-66. 2008
    ..Protein cross-linking and aggregation are important molecular processes in Alzheimer's disease (AD), and tissue transglutaminase (tTG) catalyzes protein cross-linking...
  4. ncbi request reprint Preservation of brain nerve growth factor in mild cognitive impairment and Alzheimer disease
    Elliott J Mufson
    Department of Neurological Sciences, Rush Presbyterian St Luke s Medical Center, 2242 W Harrison Street, Chicago, IL 60612, USA
    Arch Neurol 60:1143-8. 2003
    ..The status of nerve growth factor (NGF) levels during the prodromal phase of Alzheimer disease (AD), characterized by mild cognitive impairment (MCI), remains unknown...
  5. pmc Hippocampal proNGF signaling pathways and β-amyloid levels in mild cognitive impairment and Alzheimer disease
    Elliott J Mufson
    Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA
    J Neuropathol Exp Neurol 71:1018-29. 2012
    ..These findings suggest that alterations in the hippocampal NGF signaling pathway in MCI and AD favor proNGF-mediated proapoptotic pathways, and that this is independent of Aβ accumulation during AD progression...
  6. ncbi request reprint m2 muscarinic acetylcholine receptor-immunoreactive neurons are not reduced within the nucleus basalis in Alzheimer's disease: relationship with cholinergic and galaninergic perikarya
    E J Mufson
    Department of Neurological Sciences, Rush Presbyterian St Luke s Medical Center, Chicago, Illinois 60612, USA
    J Comp Neurol 392:313-29. 1998
    ..Thus, the reduced levels of the m2 receptor seen in AD cortex probably reflect changes in other neuronal populations...
  7. pmc Preservation of cortical sortilin protein levels in MCI and Alzheimer's disease
    Elliott J Mufson
    Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA
    Neurosci Lett 471:129-33. 2010
    ..These findings are relevant to the development of NGF drug therapy for the treatment of dementia...
  8. pmc Cholinergic system during the progression of Alzheimer's disease: therapeutic implications
    Elliott J Mufson
    Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA
    Expert Rev Neurother 8:1703-18. 2008
    ..Drugs treating the multiple pathologies and clinical symptoms in AD (e.g., M1 cholinoceptor and/or galaninergic drugs) should be considered for a more comprehensive treatment approach for cholinergic dysfunction...
  9. ncbi request reprint Nerve growth factor: structure, function and therapeutic implications for Alzheimer's disease
    Shivanand P Lad
    Department of Neurological Sciences and Rush Alzheimer s Disease Center, Rush Presbyterian St Luke s Medical School, Chicago, IL 60612, USA
    Curr Drug Targets CNS Neurol Disord 2:315-34. 2003
    ....
  10. ncbi request reprint Human cholinergic basal forebrain: chemoanatomy and neurologic dysfunction
    Elliott J Mufson
    Department of Neurological Sciences and Alzheimer s Disease Center, Rush Presbyterian St Luke s Medical Center, Tech 2000, 2242 West Harrison St, Suite 200, Chicago, IL 60612, USA
    J Chem Neuroanat 26:233-42. 2003
    ..These observations indicate the complexity of the chemoanatomy of the human CBF and suggest that multiple factors play different roles in its dysfunction in aging and AD...
  11. ncbi request reprint Galanin in Alzheimer disease
    Scott E Counts
    Department of Neurological Sciences, Rush Presbyterian St Luke s Medical Center, 2242 West Harrison Street, Chicago, IL 60612, USA
    Mol Interv 3:137-56. 2003
    ..Thus, GAL may also be neuroprotective for AD. Further elucidation of GAL activity in selectively vulnerable brain regions will help gauge the therapeutic potential of GALR ligands for the treatment of AD...
  12. ncbi request reprint Cholinotrophic molecular substrates of mild cognitive impairment in the elderly
    Elliott J Mufson
    Department of Neurological Sciences, Rush University Medical School, Chicago, IL 60612, USA
    Curr Alzheimer Res 4:340-50. 2007
    ..These findings support the concept that from a neurotrophic pathobiologic perspective, MCI is already early AD...
  13. ncbi request reprint Neuronal gene expression profiling: uncovering the molecular biology of neurodegenerative disease
    Elliott J Mufson
    Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA
    Prog Brain Res 158:197-222. 2006
    ..This chapter will review how regional and single cell gene array technologies have advanced our understanding of the genetics of human neurological disease...
  14. ncbi request reprint Galanin plasticity in the cholinergic basal forebrain in Alzheimer's disease and transgenic mice
    Elliott J Mufson
    Department of Neurological Sciences, Rush University Medical Center, 1735 West Harrison Street, Suite 300, Chicago, IL 60612, USA
    Neuropeptides 39:233-7. 2005
    ..Understanding GALs role in the clinical and pathological features of AD, may lead to novel drug treatments for this disease...
  15. pmc Inability of plasma and urine F2A-isoprostane levels to differentiate mild cognitive impairment from Alzheimer's disease
    Elliott J Mufson
    Department of Neurological Sciences, Rush University Medical Center, Chicago, IL, USA
    Neurodegener Dis 7:139-42. 2010
    ..The plasma lipid peroxidation enzyme F2-isoprostane has been suggested as a biomarker to detect the progression from mild cognitive impairment (MCI) to AD...
  16. ncbi request reprint Galanin receptor plasticity within the nucleus basalis in early and late Alzheimer's disease: an in vitro autoradiographic analysis
    E J Mufson
    Deptartment of Neurological Sciences, Rush Presbyterian St Luke s Medical Center, Tech 2000, 2242 West Harrison, 60612, Chicago, IL, USA
    Neuropharmacology 39:1404-12. 2000
    ..These observations show that the occurrence of overexpression of GALRs coincide with earlier reports showing galaninergic fibers hyperinnervating surviving cholinergic basal forebrain neurons in late stage AD...
  17. ncbi request reprint Estrogen receptor immunoreactivity within subregions of the rat forebrain: neuronal distribution and association with perikarya containing choline acetyltransferase
    E J Mufson
    Department of Neurological Sciences, Center for Brain Repair, Rush Alzheimer s Disease Center, Rush Presbyterian St Luke s Medical Center, Chicago, IL, USA
    Brain Res 849:253-74. 1999
    ..These observations suggest that estrogen effects a subpopulation of cholinergic basal forebrain neurons and may provide insight into the biologic actions of this steroid in Alzheimer's disease...
  18. ncbi request reprint Loss of nucleus basalis neurons containing trkA immunoreactivity in individuals with mild cognitive impairment and early Alzheimer's disease
    E J Mufson
    Department of Neurological Sciences, Rush Alzheimer s Disease Center, Rush Presbyterian St Luke s Medical Center, Chicago, Illinois 60612, USA
    J Comp Neurol 427:19-30. 2000
    ..These data indicate that alterations in the number of nucleus basalis neurons containing trkA immunoreactivity occurs early and are not accelerated from the transition from MCI to mild AD...
  19. ncbi request reprint Galanin expression within the basal forebrain in Alzheimer's disease. Comments on therapeutic potential
    E J Mufson
    Department of Neurological Sciences, Rush Presbyterian St Lukes Medical Center, Chicago, Illinois 60612, USA
    Ann N Y Acad Sci 863:291-304. 1998
    ..These observations suggest that the development of a potent galanin antagonist would be a useful step towards the successful pharmacologic treatment of Alzheimer's disease...
  20. ncbi request reprint Distribution and retrograde transport of trophic factors in the central nervous system: functional implications for the treatment of neurodegenerative diseases
    E J Mufson
    Research Center for Brain Repair, Department of Neurological Sciences, Rush Presbyterian Luke s Medical Center, Chicago, IL 60612, USA
    Prog Neurobiol 57:451-84. 1999
    ..Since select neurotrophins traffic anterogradely and retrogradely within the nervous system, these proteins could be used to treat neurological diseases such as Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis...
  21. pmc Mild cognitive impairment: pathology and mechanisms
    Elliott J Mufson
    Department of Neurological Sciences, Rush University Medical Center, 1735 West Harrison St, Suite 300, Chicago, IL 60612, USA
    Acta Neuropathol 123:13-30. 2012
    ..In fact, it can be argued that neuronal degeneration initiated at different levels of the central nervous system drives cognitive decline as a final common pathway at this stage of the dementing disease process...
  22. ncbi request reprint Gene expression profiles of cholinergic nucleus basalis neurons in Alzheimer's disease
    Elliott J Mufson
    Department of Neurological Sciences, Rush Alzheimer s Disease Research Center, Rush Presbyterian St Luke s Medical Center, Chicago, IL 60612, USA
    Neurochem Res 27:1035-48. 2002
    ..Thus, anterior NB neurons undergo selective alterations in gene expression in AD. These results may provide clues to the molecular pathogenesis of NB neuronal degeneration during AD...
  23. ncbi request reprint Loss of basal forebrain P75(NTR) immunoreactivity in subjects with mild cognitive impairment and Alzheimer's disease
    Elliott J Mufson
    Department of Neurological Sciences, Rush Presbyterian St Luke s Medical Center, Chicago, Illinois 60612, USA
    J Comp Neurol 443:136-53. 2002
    ..Although there was no difference in p75(NTR) CBF cell reduction between MCI and AD, it remains to be determined whether these findings lend support to the hypothesis that MCI is a prodromal stage of AD...
  24. ncbi request reprint Reduction of cortical TrkA but not p75(NTR) protein in early-stage Alzheimer's disease
    Scott E Counts
    Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA
    Ann Neurol 56:520-31. 2004
    ..The selective reduction of cortical TrkA levels relative to p75(NTR) may have important consequences for cholinergic NB function during the transition from MCI to AD...
  25. pmc Galanin hyperinnervation upregulates choline acetyltransferase expression in cholinergic basal forebrain neurons in Alzheimer's disease
    Scott E Counts
    Department of Neurological Sciences, Rush University Medical Center, Chicago, Ill 60612, USA
    Neurodegener Dis 5:228-31. 2008
    ..Fibers containing galanin (GAL) enlarge and hyperinnervate cholinergic basal forebrain (CBF) nucleus basalis (NB) neurons in late-stage Alzheimer's disease (AD), yet the physiological consequences of this phenomenon are unclear...
  26. pmc Cholinergic forebrain degeneration in the APPswe/PS1DeltaE9 transgenic mouse
    Sylvia E Perez
    Department of Neurological Sciences, Alla V and Solomon Jesmer Chair in Aging, Rush University Medical Center, 1735 W Harrison Street, Suite 300, Chicago, IL 60612, USA
    Neurobiol Dis 28:3-15. 2007
    ....
  27. ncbi request reprint Differential expression of synaptic proteins in the frontal and temporal cortex of elderly subjects with mild cognitive impairment
    Scott E Counts
    Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA
    J Neuropathol Exp Neurol 65:592-601. 2006
    ....
  28. ncbi request reprint Galanin fiber hypertrophy within the cholinergic nucleus basalis during the progression of Alzheimer's disease
    Scott E Counts
    Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA
    Dement Geriatr Cogn Disord 21:205-14. 2006
    ..These observations indicate that GAL hypertrophy within the anterior NB subfield is a late-stage AD response, which may play a role in regulating the cholinergic tone of remaining basocortical projection neurons...
  29. pmc Nurr1 in Parkinson's disease and related disorders
    Yaping Chu
    Department of Neurological Science, Rush University Medical Center, Chicago, Illinois 60612, USA
    J Comp Neurol 494:495-514. 2006
    ..These data demonstrate that Nurr1 deficiency in dopaminergic neurons is associated with the intracellular pathology in both synucleinopathies and tauopathies...
  30. pmc Cortical M1 receptor concentration increases without a concomitant change in function in Alzheimer's disease
    Cassia R Overk
    Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA
    J Chem Neuroanat 40:63-70. 2010
    ....
  31. ncbi request reprint Alpha7 nicotinic receptor up-regulation in cholinergic basal forebrain neurons in Alzheimer disease
    Scott E Counts
    Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA
    Arch Neurol 64:1771-6. 2007
    ..Although alterations in these AChRs occur in the AD cortex, there is little information detailing whether defects in nAChR and mAChR gene expression occur in cholinergic NB neurons during disease progression...
  32. pmc Noradrenaline activation of neurotrophic pathways protects against neuronal amyloid toxicity
    Scott E Counts
    Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois, USA
    J Neurochem 113:649-60. 2010
    ....
  33. pmc Cholinotrophic basal forebrain system alterations in 3xTg-AD transgenic mice
    Sylvia E Perez
    Department of Neurological Sciences, Rush University Medical Center, 1735 West Harrison Street, Suite 300, Chicago, IL 60612, USA
    Neurobiol Dis 41:338-52. 2011
    ..These data demonstrate that cholinotrophic alterations in 3xTg-AD mice are age- and gender-dependent and more pronounced in the hippocampus, a structure more severely affected by Aβ plaque pathology...
  34. pmc Galanin fiber hyperinnervation preserves neuroprotective gene expression in cholinergic basal forebrain neurons in Alzheimer's disease
    Scott E Counts
    Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA
    J Alzheimers Dis 18:885-96. 2009
    ..Hence, GAL fiber hyperinnervation appears to preserve the expression of genes subserving multiple neuroprotective pathways suggesting that GAL overexpression regulates CBF neuron survival in AD...
  35. pmc Brainstem Alzheimer's-like pathology in the triple transgenic mouse model of Alzheimer's disease
    Cassia R Overk
    Department of Neurological Sciences, Rush University Medical Center, 1735 W Harrison Street, Suite 300, Chicago, IL 60612, USA
    Neurobiol Dis 35:415-25. 2009
    ..Dual labeling revealed a few Abeta- and tau-positive neurons. Plaques occurred only in the pons of female 3xTgAD mice starting at 9 months. 3xTgAD mice provide a platform to define in vivo mechanisms of Abeta and tau brainstem pathology...
  36. pmc Beta-amyloid deposition and functional impairment in the retina of the APPswe/PS1DeltaE9 transgenic mouse model of Alzheimer's disease
    Sylvia E Perez
    Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois, USA
    Invest Ophthalmol Vis Sci 50:793-800. 2009
    ..To determine whether beta-amyloid (Abeta) deposition affects the structure and function of the retina of the APPswe/PS1DeltaE9 transgenic (tg) mouse model of Alzheimer's disease...
  37. ncbi request reprint Improved detection of substantia nigra pathology in Alzheimer's disease
    Julie A Schneider
    Rush Alzheimer s Disease Center, Rush University and Rush Presbyterian St Luke s Medical Center, Chicago, Illinois, USA
    J Histochem Cytochem 50:99-106. 2002
    ..We show that detection of nigra pathology is influenced by histological method. Clinicopathological studies using these methods are needed to determine the role of nigral pathology in AD...
  38. ncbi request reprint Effects of estrogen replacement therapy on cholinergic basal forebrain neurons and cortical cholinergic innervation in young and aged ovariectomized rhesus monkeys
    Katie Kompoliti
    Department of Neurological Sciences, Rush University Medical Center, Rush University, Chicago, Illinois 60612, USA
    J Comp Neurol 472:193-207. 2004
    ....
  39. ncbi request reprint Nigrostriatal dysfunction in familial Alzheimer's disease-linked APPswe/PS1DeltaE9 transgenic mice
    Sylvia E Perez
    Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois 60612, USA
    J Neurosci 25:10220-9. 2005
    ..These findings show a close association between amyloid deposition and nigrostriatal pathology and suggest that altered FAD-linked amyloid metabolism impairs, at least in part, the function of dopaminergic neurons...
  40. ncbi request reprint Age-related decreases in Nurr1 immunoreactivity in the human substantia nigra
    Yaping Chu
    Department of Neurological Sciences, Rush Presbyterian St Luke s Medical Center, Chicago, Illinois 60612, USA
    J Comp Neurol 450:203-14. 2002
    ..These data demonstrate that age-related decline of DA phenotypic markers is associated with down-regulation of Nurr1 expression in the SN...
  41. ncbi request reprint Galanin inhibits tyrosine hydroxylase expression in midbrain dopaminergic neurons
    Scott E Counts
    Department of Neurological Sciences and Pharmacology, Rush Presbyterian St Luke s Medical Center, Chicago, Illinois 60612, USA
    J Neurochem 83:442-51. 2002
    ..GAL inhibition of midbrain DA activity may involve a GALR1- mediated reduction of TH in midbrain dopaminergic neurons...
  42. pmc DHA diet reduces AD pathology in young APPswe/PS1 Delta E9 transgenic mice: possible gender effects
    Sylvia E Perez
    Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois 60612, USA
    J Neurosci Res 88:1026-40. 2010
    ..Finally, in vitro DHA treatment prevented amyloid toxicity in cell cultures. Our findings support the concept that increased DHA consumption may play and important role in reducing brain insults in female AD patients...
  43. ncbi request reprint Excitotoxic and metabolic damage to the rodent striatum: role of the P75 neurotrophin receptor and glial progenitors
    Rose Hanbury
    Research Center for Brain Repair and Department of Neurological Sciences, Rush Presbyterian Medical Center, 2242 West Harrison Street, Chicago, IL 60612, USA
    J Comp Neurol 444:291-305. 2002
    ..The expression of the p75(NTR) receptor after these chemical lesions support the concept that this receptor plays a role in the initiation of endogenous cellular events associated with CNS injury...
  44. ncbi request reprint Distribution of estrogen receptor alpha and beta immunoreactive profiles in the postnatal rat brain
    Sylvia E Perez
    Neurological Sciences, Rush Presbyterian St Luke s Medical Center, Chicago, IL 60612, USA
    Brain Res Dev Brain Res 145:117-39. 2003
    ..The presence of ERs in diverse brain regions through early postnatal periods supports a potential role for estrogens in neural differentiation...
  45. pmc Selective inhibition of NF-kappaB activation prevents dopaminergic neuronal loss in a mouse model of Parkinson's disease
    Anamitra Ghosh
    Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA
    Proc Natl Acad Sci U S A 104:18754-9. 2007
    ..These findings were specific because mutated NBD peptide had no effect. We conclude that selective inhibition of NF-kappaB activation by NBD peptide may be of therapeutic benefit for PD patients...
  46. ncbi request reprint Galanin receptor over-expression within the amygdala in early Alzheimer's disease: an in vitro autoradiographic analysis
    Sylvia Perez
    Department of Neurological Science, Rush Presbyterian, St Luke s Medical Center, Chicago, IL 60612, USA
    J Chem Neuroanat 24:109-16. 2002
    ..The over-expression of GALRs in subfields of the amygdaloid early in AD suggests that galaninergic systems play a key role in limbic related behavioral changes during the disease process...
  47. ncbi request reprint Distribution of high affinity choline transporter immunoreactivity in the primate central nervous system
    Laura Kus
    Department of Neurological Sciences, Rush Presbyterian St Luke s Medical Center, Chicago, Illinois 60612
    J Comp Neurol 463:341-57. 2003
    ..The present observations indicate that the present CHT antibody labels cholinergic structures within the primate CNS and provides an additional marker for the investigation of cholinergic neuronal function in aging and disease...
  48. ncbi request reprint RNA amplification of bromodeoxyuridine labeled newborn neurons in the monkey hippocampus
    Scott E Counts
    Department of Neurological Sciences, Alla and Solomon Jesmer Chair in Aging, Rush University Medical Center, 1735 W Harrison Street, Suite 300, Chicago, IL, USA
    J Neurosci Methods 144:197-201. 2005
    ..The present study demonstrates for the first time that BrdU immunohistochemisty is compatable with gene array technology in the primate hippocampus to evaluate subclasses of genes in newborn neurons...
  49. ncbi request reprint Neuronal cell death is preceded by cell cycle events at all stages of Alzheimer's disease
    Yan Yang
    Alzheimer Research Laboratory, University Hospitals of Cleveland and Department of Neurosciences, Case Western Reserve University, School of Medicine, Cleveland, Ohio 44106, USA
    J Neurosci 23:2557-63. 2003
    ..The implication of the findings for human clinical trials is discussed...
  50. ncbi request reprint Cholinergic plasticity in hippocampus of individuals with mild cognitive impairment: correlation with Alzheimer's neuropathology
    Milos D Ikonomovic
    Department of Neurology, University of Pittsburgh School of Medicine, PA 15213, USA
    J Alzheimers Dis 5:39-48. 2003
    ..Moreover, the present findings suggest that the short-term memory loss observed in MCI is not caused by cholinergic deficits; it more likely relates to disrupted entorhinal-hippocampal connectivity...
  51. ncbi request reprint Single-cell gene expression analysis: implications for neurodegenerative and neuropsychiatric disorders
    Stephen D Ginsberg
    Center for Dementia Research, Nathan Kline Institute, New York University School of Medicine, Orangeburg, New York 10962, USA
    Neurochem Res 29:1053-64. 2004
    ..This focused review illustrates the potential power of single-cell gene expression studies within the CNS in relation to neurodegenerative and neuropsychiatric disorders such as Alzheimer's disease (AD) and schizophrenia, respectively...
  52. ncbi request reprint Upregulation of choline acetyltransferase activity in hippocampus and frontal cortex of elderly subjects with mild cognitive impairment
    Steven T DeKosky
    Department of Neurology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA
    Ann Neurol 51:145-55. 2002
    ..The upregulation in frontal cortex and hippocampal ChAT activity could be an important factor in preventing the transition of MCI subjects to AD...
  53. ncbi request reprint Shift in the ratio of three-repeat tau and four-repeat tau mRNAs in individual cholinergic basal forebrain neurons in mild cognitive impairment and Alzheimer's disease
    Stephen D Ginsberg
    Center for Dementia Research, Nathan Kline Institute, Orangeburg, New York 10962, USA
    J Neurochem 96:1401-8. 2006
    ..A shift in 3Rtau to 4Rtau may precipitate a cascade of events in the selective vulnerability of neurons, ultimately leading to frank neurofibrillary tangle (NFT) formation in tauopathies including AD...
  54. ncbi request reprint Estrogen restores cognition and cholinergic phenotype in an animal model of Down syndrome
    Ann Charlotte E Granholm
    Department of Physiology and Neuroscience, Medical University of South Carolina, Charleston, SC 29425, USA
    Physiol Behav 77:371-85. 2002
    ..The findings also indicate that estrogen may act, at least partially, via endogenous growth factors. Collectively, the data suggest that ERT may be a viable therapeutic approach for women with DS coupled with dementia...
  55. ncbi request reprint Galanin overexpressing transgenic mice
    Jacqueline N Crawley
    Section on Behavioral Genomics, National Institute of Mental Health, Bethesda, MD 20815, USA
    Neuropeptides 36:145-56. 2002
    ..GAL-tg represent a new model for investigating the biological actions of endogenous galanin, and for testing novel therapeutics based on galanin receptor ligands...
  56. ncbi request reprint Precursor form of brain-derived neurotrophic factor and mature brain-derived neurotrophic factor are decreased in the pre-clinical stages of Alzheimer's disease
    Shiyong Peng
    Department of Psychiatry and Behavioural Neurosciences, McMaster University, Hamilton, Ontario, Canada
    J Neurochem 93:1412-21. 2005
    ....
  57. ncbi request reprint Parahippocampal tau pathology in healthy aging, mild cognitive impairment, and early Alzheimer's disease
    Thomas W Mitchell
    Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
    Ann Neurol 51:182-9. 2002
    ....
  58. pdf Down regulation of trk but not p75NTR gene expression in single cholinergic basal forebrain neurons mark the progression of Alzheimer's disease
    Stephen D Ginsberg
    Center for Dementia Research, Nathan Kline Institute, New York University School of Medicine, Orangeburg, USA
    J Neurochem 97:475-87. 2006
    ..In contrast, there is a lack of regulation of p75(NTR) expression. Thus, trk defects may be a molecular marker for the transition from no cognitive impairment (NCI) to MCI, and from MCI to frank AD...
  59. ncbi request reprint Increased metabolic activity in nucleus basalis of Meynert neurons in elderly individuals with mild cognitive impairment as indicated by the size of the Golgi apparatus
    Elisabeth J G Dubelaar
    Netherlands Institute for Brain Research, Amsterdam, The Netherlands
    J Neuropathol Exp Neurol 65:257-66. 2006
    ..The larger NBM neuronal GA size seen in MCI suggests increased metabolic activity, associated with both the clinical progression from NCI to MCI, and with the early stages of AD pathology...
  60. pmc Activation of caspase-6 in aging and mild cognitive impairment
    Steffen Albrecht
    The Bloomfield Center for Research in Aging, Lady Davis Institute for Medical Research, The Sir Mortimer B Davis Jewish, General Hospital, 3755 Ch Cote Ste Catherine, Montreal, QC, Canada
    Am J Pathol 170:1200-9. 2007
    ..Program No. 80.9. 2005 Abstract Viewer/Itinerary Planner. Washington, DC: Society for Neuroscience. Online), we suggest that active Csp6 could be an early instigator of neuronal dysfunction...
  61. ncbi request reprint Reduction of choline acetyltransferase activity in primary visual cortex in mild to moderate Alzheimer's disease
    Milos D Ikonomovic
    Department of Neurology and the Alzheimer s Disease Research Center, University of Pittsburgh, Pittsburgh, PA 25213, USA
    Arch Neurol 62:425-30. 2005
    ..Cholinergic deficits in the primary visual cortex (PVC) may underlie some of the abnormalities in visual processing and global cognitive performance in Alzheimer's disease (AD)...
  62. pmc Neuronal LR11/sorLA expression is reduced in mild cognitive impairment
    Kristen L Sager
    Center for Neurodegenerative Disease, Emory University, Atlanta, GA 30322, USA
    Ann Neurol 62:640-7. 2007
    ....
  63. ncbi request reprint Superior frontal cortex cholinergic axon density in mild cognitive impairment and early Alzheimer disease
    Milos D Ikonomovic
    Department of Neurology, University of Pittsburgh School of Medicine, 341 Fifth Ave, Ste 811, Pittsburgh, PA 15213, USA
    Arch Neurol 64:1312-7. 2007
    ....
  64. ncbi request reprint Increased proNGF levels in subjects with mild cognitive impairment and mild Alzheimer disease
    Shiyong Peng
    Department of Psychiatry and Behavioural Neurosciences, McMaster University, Hamilton, Ontario, Canada
    J Neuropathol Exp Neurol 63:641-9. 2004
    ..These findings demonstrate that proNGF levels increase during the preclinical stage of AD and may reflect an early biological marker for the onset of AD...
  65. pmc Single cell gene expression profiling in Alzheimer's disease
    Stephen D Ginsberg
    Center for Dementia Research, Nathan Kline Institute, Orangeburg, NY 10962, USA
    NeuroRx 3:302-18. 2006
    ....
  66. ncbi request reprint Contribution of changes in ubiquitin and myelin basic protein to age-related cognitive decline
    Deng Shun Wang
    Department of Neuroscience and Pathology Neuropathology, Birdsall 317, Mayo Clinic Jacksonville, 4500 Sam Pablo Road, Jacksonville, FL 32224, USA
    Neurosci Res 48:93-100. 2004
    ..An age-related decrease in MBP immunoreactivity was detected in NCI cases (r=0.71). These results support the hypothesis that white matter pathology may contribute to age-associated decline in cognition...
  67. pmc Nanoparticle-based detection in cerebral spinal fluid of a soluble pathogenic biomarker for Alzheimer's disease
    Dimitra G Georganopoulou
    Department of Chemistry and Institute of Nanotechnology, Northwestern University, 2145 Sheridan Road, Evanston, IL 60208, USA
    Proc Natl Acad Sci U S A 102:2273-6. 2005
    ..This study is a step toward a diagnostic tool, based on soluble pathogenic markers for the debilitating disease...
  68. pmc Neuronal sorting protein-related receptor sorLA/LR11 regulates processing of the amyloid precursor protein
    Olav M Andersen
    Max Delbrueck Center for Molecular Medicine, D 13125 Berlin, Germany
    Proc Natl Acad Sci U S A 102:13461-6. 2005
    ..Consequently, reduced receptor expression in the human brain may increase Abeta production and plaque formation and promote spontaneous AD...
  69. ncbi request reprint Hippocampal synaptic loss in early Alzheimer's disease and mild cognitive impairment
    Stephen W Scheff
    Sanders Brown Center on Aging and the Alzheimer s Disease Research Center, University of Kentucky College of Medicine, 101 Sanders Brown, Lexington, KY 40536 0230, USA
    Neurobiol Aging 27:1372-84. 2006
    ..This study supports the concept that synapse loss is an early event in the disease process and suggests that MCI may be a transition stage between eAD and NCI with synaptic loss a structural correlate involved in cognitive decline...

Research Grants20

  1. GALANIN IN ALZHEIMER'S DISEASE
    Elliott Mufson; Fiscal Year: 2007
    ..g., GAL ligands) for the reduction of amyloid toxicity in Alzheimer's disease. ..
  2. TRAINING IN AGE-RELATED NEURODEGENERATIVE DISEASES
    Elliott Mufson; Fiscal Year: 2007
    ..Finally the program will provide a broad-base of knowledge on neurodegenerative disorders as well as other instruction important for enhancing the interpersonal and professional skills of our trainees. ..
  3. GALANIN IN ALZHEIMER'S DISEASE
    Elliott Mufson; Fiscal Year: 2009
    ..g., GAL ligands) for the reduction of amyloid toxicity in Alzheimer's disease. ..
  4. GALANIN IN ALZHEIMER'S DISEASE
    Elliott Mufson; Fiscal Year: 1999
    ..Furthermore, these data may suggest avenues for pharmacological therapies aimed at retarding intellectual deterioration in AD. ..
  5. GALANIN IN ALZHEIMER'S DISEASE
    Elliott Mufson; Fiscal Year: 1991
    ..Furthermore, these data my suggest avenues for the development of new pharmacological therapies as a means of retarding intellectual deterioration in dementia...
  6. GALANIN IN ALZHEIMER'S DISEASE
    Elliott Mufson; Fiscal Year: 1992
    ..Furthermore, these data my suggest avenues for the development of new pharmacological therapies as a means of retarding intellectual deterioration in dementia...
  7. GALANIN IN ALZHEIMER'S DISEASE
    Elliott Mufson; Fiscal Year: 1993
    ..Furthermore, these data my suggest avenues for the development of new pharmacological therapies as a means of retarding intellectual deterioration in dementia...
  8. Galanin in Alzheimer's Disease
    ELLIOTT JAY MUFSON; Fiscal Year: 2010
    ..g., GAL ligands) for the reduction of amyloid toxicity in Alzheimer's disease. ..