Milos D Ikonomovic

Summary

Affiliation: University of Pittsburgh
Country: USA

Publications

  1. pmc Early AD pathology in a [C-11]PiB-negative case: a PiB-amyloid imaging, biochemical, and immunohistochemical study
    Milos D Ikonomovic
    Department of Neurology, University of Pittsburgh School of Medicine, 200 Lothrop Street BST S521, Pittsburgh, PA 15213 USA
    Acta Neuropathol 123:433-47. 2012
  2. pmc Precuneus amyloid burden is associated with reduced cholinergic activity in Alzheimer disease
    M D Ikonomovic
    Department of Neurology, University of Pittsburgh, 200 Lothrop Street BST S521, Pittsburgh, PA 15213, USA
    Neurology 77:39-47. 2011
  3. pmc Increased 5-lipoxygenase immunoreactivity in the hippocampus of patients with Alzheimer's disease
    Milos D Ikonomovic
    Department of Neurology, University of Pittsburgh School of Medicine, BSTWR S 521, Pittsburgh, PA 15261, USA
    J Histochem Cytochem 56:1065-73. 2008
  4. pmc Post-mortem correlates of in vivo PiB-PET amyloid imaging in a typical case of Alzheimer's disease
    Milos D Ikonomovic
    Department of Neurology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA
    Brain 131:1630-45. 2008
  5. ncbi request reprint Caspase inhibition therapy abolishes brain trauma-induced increases in Abeta peptide: implications for clinical outcome
    Eric E Abrahamson
    Department of Neurology, University of Pittsburgh School of Medicine, 3471 Fifth Avenue, Suite 811, 15213, USA
    Exp Neurol 197:437-50. 2006
  6. ncbi request reprint The binding of 2-(4'-methylaminophenyl)benzothiazole to postmortem brain homogenates is dominated by the amyloid component
    William E Klunk
    Laboratory of Molecular Neuropharmacology, Department of Psychiatry, Western Psychiatric Institute and Clinic, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15213, USA
    J Neurosci 23:2086-92. 2003
  7. ncbi request reprint Apolipoprotein D is a component of compact but not diffuse amyloid-beta plaques in Alzheimer's disease temporal cortex
    Purnima P Desai
    Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA 15261, USA
    Neurobiol Dis 20:574-82. 2005
  8. pmc Cortical alpha7 nicotinic acetylcholine receptor and beta-amyloid levels in early Alzheimer disease
    Milos D Ikonomovic
    Department of Neurology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA
    Arch Neurol 66:646-51. 2009
  9. ncbi request reprint Alzheimer's pathology in human temporal cortex surgically excised after severe brain injury
    Milos D Ikonomovic
    Department of Neurology, University of Pittsburgh School of Medicine, 3471 Fifth Avenue, Pittsburgh, PA 15213, USA
    Exp Neurol 190:192-203. 2004
  10. ncbi request reprint Binding of the positron emission tomography tracer Pittsburgh compound-B reflects the amount of amyloid-beta in Alzheimer's disease brain but not in transgenic mouse brain
    William E Klunk
    Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, USA
    J Neurosci 25:10598-606. 2005

Detail Information

Publications32

  1. pmc Early AD pathology in a [C-11]PiB-negative case: a PiB-amyloid imaging, biochemical, and immunohistochemical study
    Milos D Ikonomovic
    Department of Neurology, University of Pittsburgh School of Medicine, 200 Lothrop Street BST S521, Pittsburgh, PA 15213 USA
    Acta Neuropathol 123:433-47. 2012
    ..Studies in greater numbers of [C-11]PiB PET autopsy cases are needed to define the Aβ concentration and [H-3]PiB binding levels required to produce a positive [C-11]PiB PET signal...
  2. pmc Precuneus amyloid burden is associated with reduced cholinergic activity in Alzheimer disease
    M D Ikonomovic
    Department of Neurology, University of Pittsburgh, 200 Lothrop Street BST S521, Pittsburgh, PA 15213, USA
    Neurology 77:39-47. 2011
    ..This study examined the relationship between postmortem precuneus cholinergic enzyme activity, Pittsburgh compound B (PiB) binding, and soluble amyloid-β concentration in mild cognitive impairment (MCI) and Alzheimer disease (AD)...
  3. pmc Increased 5-lipoxygenase immunoreactivity in the hippocampus of patients with Alzheimer's disease
    Milos D Ikonomovic
    Department of Neurology, University of Pittsburgh School of Medicine, BSTWR S 521, Pittsburgh, PA 15261, USA
    J Histochem Cytochem 56:1065-73. 2008
    ..The relationship between elevated intracellular 5-LOX and hallmark AD pathological lesions provides further evidence that neuroinflammatory pathways contribute to the pathogenesis of AD...
  4. pmc Post-mortem correlates of in vivo PiB-PET amyloid imaging in a typical case of Alzheimer's disease
    Milos D Ikonomovic
    Department of Neurology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA
    Brain 131:1630-45. 2008
    ..The strong direct correlation of in vivo PiB retention with region-matched quantitative analyses of Abeta plaques in the same subject supports the validity of PiB-PET imaging as a method for in vivo evaluation of Abeta plaque burden...
  5. ncbi request reprint Caspase inhibition therapy abolishes brain trauma-induced increases in Abeta peptide: implications for clinical outcome
    Eric E Abrahamson
    Department of Neurology, University of Pittsburgh School of Medicine, 3471 Fifth Avenue, Suite 811, 15213, USA
    Exp Neurol 197:437-50. 2006
    ....
  6. ncbi request reprint The binding of 2-(4'-methylaminophenyl)benzothiazole to postmortem brain homogenates is dominated by the amyloid component
    William E Klunk
    Laboratory of Molecular Neuropharmacology, Department of Psychiatry, Western Psychiatric Institute and Clinic, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15213, USA
    J Neurosci 23:2086-92. 2003
    ..Finally, BTA-1 did not appear to bind significantly to common neuroreceptors or transporter sites. These data suggest that the binding of BTA-1 to AD brain is dominated by a specific interaction with Abeta amyloid deposits...
  7. ncbi request reprint Apolipoprotein D is a component of compact but not diffuse amyloid-beta plaques in Alzheimer's disease temporal cortex
    Purnima P Desai
    Department of Human Genetics, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA 15261, USA
    Neurobiol Dis 20:574-82. 2005
    ..Elevated apoD in AD brain may influence Abeta aggregation, or facilitate phagocytosis and transport of Abeta fibrils from plaques to cerebral vasculature...
  8. pmc Cortical alpha7 nicotinic acetylcholine receptor and beta-amyloid levels in early Alzheimer disease
    Milos D Ikonomovic
    Department of Neurology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA
    Arch Neurol 66:646-51. 2009
    ..To examine alpha7 nicotinic acetylcholine receptor (nAChR) binding and beta-amyloid (Abeta) peptide load in superior frontal cortex (SFC) across clinical and neuropathological stages of Alzheimer disease (AD)...
  9. ncbi request reprint Alzheimer's pathology in human temporal cortex surgically excised after severe brain injury
    Milos D Ikonomovic
    Department of Neurology, University of Pittsburgh School of Medicine, 3471 Fifth Avenue, Pittsburgh, PA 15213, USA
    Exp Neurol 190:192-203. 2004
    ....
  10. ncbi request reprint Binding of the positron emission tomography tracer Pittsburgh compound-B reflects the amount of amyloid-beta in Alzheimer's disease brain but not in transgenic mouse brain
    William E Klunk
    Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, USA
    J Neurosci 25:10598-606. 2005
    ....
  11. ncbi request reprint Association of increased cortical soluble abeta42 levels with diffuse plaques after severe brain injury in humans
    Steven T DeKosky
    Department of Neurology, University of Pittsburgh, 3471 Fifth Ave, Suite 811, Pittsburgh, PA 15213, USA
    Arch Neurol 64:541-4. 2007
    ..Changes in soluble Abeta levels and their relationship to Abeta plaque formation following TBI are unknown...
  12. ncbi request reprint X-34 labeling of abnormal protein aggregates during the progression of Alzheimer's disease
    Milos D Ikonomovic
    Department of Neurology and Psychiatry, University of Pittsburgh, Pennsylvania 15213, USA
    Methods Enzymol 412:123-44. 2006
    ....
  13. pmc β-Amyloid 42/40 ratio and kalirin expression in Alzheimer disease with psychosis
    Patrick S Murray
    Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA
    Neurobiol Aging 33:2807-16. 2012
    ..These findings suggest that increased cortical β-amyloid(1-42)/β-amyloid(1-40) ratio and decreased kalirin expression may both contribute to the pathogenesis of psychosis in AD...
  14. ncbi request reprint Effects of post-injury hypothermia and nerve growth factor infusion on antioxidant enzyme activity in the rat: implications for clinical therapies
    Steven T DeKosky
    Department of Neurology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, USA
    J Neurochem 90:998-1004. 2004
    ..These results have implications for clinical treatment of TBI, demonstrating that moderate hypothermia suppresses NGF and the antioxidant response after TBI; the latter cannot be countered by exogenous NGF administration...
  15. 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...
  16. doi request reprint Hyperphosphorylated Tau is Elevated in Alzheimer's Disease with Psychosis
    Patrick S Murray
    Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA VISN 4 Mental Illness Research, Education and Clinical Center, VA Pittsburgh Healthcare System, Pittsburgh, PA, USA
    J Alzheimers Dis 39:759-73. 2014
    ..These novel findings indicate that tau phosphorylation may be accelerated in AD with psychosis, indicating a more dynamic, exaggerated pathology in AD with psychosis. ..
  17. 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
    ....
  18. pmc Using Pittsburgh Compound B for in vivo PET imaging of fibrillar amyloid-beta
    Ann D Cohen
    Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA
    Adv Pharmacol 64:27-81. 2012
    ..Here, we will discuss the application of one of the most broadly studied and widely used Aβ imaging agents, Pittsburgh Compound-B (PiB)...
  19. pmc Amyloid deposition begins in the striatum of presenilin-1 mutation carriers from two unrelated pedigrees
    William E Klunk
    Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261, USA
    J Neurosci 27:6174-84. 2007
    ..The early, focal striatal amyloid deposition observed in these PS1 mutation carriers is often is not associated with clinical symptoms...
  20. doi request reprint Simvastatin therapy prevents brain trauma-induced increases in beta-amyloid peptide levels
    Eric E Abrahamson
    Department of Neurology, Brain Trauma Research Center, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA
    Ann Neurol 66:407-14. 2009
    ..The ability of statins to reduce post-injury A beta load and ameliorate pathological sequelae of brain injury makes them potentially effective in reducing the risk of developing Alzheimer's disease in TBI patients...
  21. 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)...
  22. ncbi request reprint Plasma and cerebrospinal fluid alpha1-antichymotrypsin levels in Alzheimer's disease: correlation with cognitive impairment
    Steven T DeKosky
    Department of Neurology and the Alzheimer s Disease Research Center, University of Pittsburgh, PA, USA
    Ann Neurol 53:81-90. 2003
    ....
  23. ncbi request reprint Time course analysis of hippocampal nerve growth factor and antioxidant enzyme activity following lateral controlled cortical impact brain injury in the rat
    Steven T DeKosky
    Department of Neurology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, USA
    J Neurotrauma 21:491-500. 2004
    ..These data demonstrate a complex temporal spectrum of antioxidant enzyme activation following secondary brain injury in the hippocampus, and suggest a selective regulatory role for NGF in this response...
  24. pmc Dendritic spine density, morphology, and fibrillar actin content surrounding amyloid-β plaques in a mouse model of amyloid-β deposition
    Caitlin M Kirkwood
    Translational Neuroscience Program, Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA
    J Neuropathol Exp Neurol 72:791-800. 2013
    ....
  25. pmc Cerebral blood flow changes after brain injury in human amyloid-beta knock-in mice
    Eric E Abrahamson
    Department of Neurology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
    J Cereb Blood Flow Metab 33:826-33. 2013
    ..Future studies examining long-term effects of simvastatin therapy on CBF and chronic neurodegenerative changes after TBI are warranted...
  26. ncbi request reprint Biochemical and molecular studies of NMDA receptor subunits NR1/2A/2B in hippocampal subregions throughout progression of Alzheimer's disease pathology
    Amanda J Mishizen-Eberz
    Laboratory of Neuronal Vulnerability and Aging, The Lankenau Institute for Medical Research, Jefferson Health System, Wynnewood, PA, USA
    Neurobiol Dis 15:80-92. 2004
    ..This investigation supports the hypothesis that alterations occur in the expression of specific NMDA receptor subunits with increasing AD pathologic severity, which is hypothesized to contribute to the vulnerability of these neurons...
  27. ncbi request reprint Increased phosphorylation of protein kinase B and related substrates after traumatic brain injury in humans and rats
    Xiaopeng Zhang
    Department of Critical Care Medicine, The Safar Center for Resuscitation Research, University of Pittsburgh School of Medicine, Pittsburgh, Pennyslvania 15260, USA
    J Cereb Blood Flow Metab 26:915-26. 2006
    ..These data show increased phosphorylation of PKB, PKB substrates, and related proteins after both experimental and clinical TBI, suggesting either activation of the PKB signaling pathway or reduced phosphatase activity in both species...
  28. ncbi request reprint 22R-hydroxycholesterol and 9-cis-retinoic acid induce ATP-binding cassette transporter A1 expression and cholesterol efflux in brain cells and decrease amyloid beta secretion
    Radosveta P Koldamova
    Department of Pharmacology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261, USA
    J Biol Chem 278:13244-56. 2003
    ..These effects of 22R-hydroxycholesterol may provide a novel strategy to decrease amyloid beta secretion and consequently reduce the amyloid burden in the brain...
  29. ncbi request reprint Changes in expression of amyloid precursor protein and interleukin-1beta after experimental traumatic brain injury in rats
    John R Ciallella
    Department of Psychiatry, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA
    J Neurotrauma 19:1555-67. 2002
    ..Our results demonstrate that both APP and IL-1beta are rapidly elevated after injury. Because of the rapidity in the IL-1beta peak increase, it may serve a role in regulation of APP expression after TBI...
  30. ncbi request reprint Alterations in hippocampal voltage-gated calcium channel alpha 1 subunit expression patterns after kainate-induced status epilepticus in aging rats
    Kevin M Kelly
    Department of Neurology, Allegheny Singer Research Institute, Allegheny General Hospital, 940 South Tower, 320 E North Avenue, Pittsburgh, PA 15212 4772, USA
    Epilepsy Res 57:15-32. 2003
    ....
  31. 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...
  32. ncbi request reprint Distribution of plasma alpha 1-antichymotrypsin levels in Alzheimer disease patients and controls and their genetic controls
    Xiaoyan Wang
    Department of Human Genetics, Graduate School of Public Health, 130 DeSoto Street, University of Pittsburgh, Pittsburgh, PA 15261, USA
    Neurobiol Aging 23:377-82. 2002
    ..In conclusion, ACT may play an important role in the AD pathogenesis and genetic variation in the ACT gene appears to have some effect on plasma ACT concentrations...