Michael T Heneka

Summary

Affiliation: University of Bonn
Country: Germany

Publications

  1. pmc Impact and Therapeutic Potential of PPARs in Alzheimer's Disease
    Michael T Heneka
    University of Bonn, Department of Neurology, Clinical Neurosciences Unit, Bonn, Germany
    Curr Neuropharmacol 9:643-50. 2011
  2. pmc Clinical symptoms and risk factors in cerebral microangiopathy patients
    Sandra Okroglic
    Department of Neurology, Clinical Neuroscience Unit, University of Bonn, Bonn, Germany
    PLoS ONE 8:e53455. 2013
  3. pmc NLRP3 is activated in Alzheimer's disease and contributes to pathology in APP/PS1 mice
    Michael T Heneka
    Clinical Neuroscience Unit, Department of Neurology, University of Bonn, Sigmund Freud Strasse 25, 53127 Bonn, Germany
    Nature 493:674-8. 2013
  4. pmc Effect of anti-inflammatory agents on transforming growth factor beta over-expressing mouse brains: a model revised
    Pierre Lacombe
    Laboratoire de Recherches C r brovasculaires, CNRS FRE 2363, Paris, France
    J Neuroinflammation 1:11. 2004
  5. pmc Norepinephrine enhances the LPS-induced expression of COX-2 and secretion of PGE2 in primary rat microglia
    Johannes C M Schlachetzki
    Department of Psychiatry and Psychotherapy, University Hospital of Freiburg, Freiburg, Germany
    J Neuroinflammation 7:2. 2010
  6. ncbi Molecular mechanisms and therapeutic application of NSAIDs and derived compounds in Alzheimer's disease
    M T Heneka
    Department of Neurology, Clinical Neurosciences, Unversity of Bonn, Sigmund Freud Str 25, 53127 Bonn, Germany
    Curr Alzheimer Res 8:115-31. 2011
  7. ncbi [Course modifying therapy of Alzheimer's dementia]
    M T Heneka
    Klinische Neurowissenschaften, Klinik und Poliklinik fur Neurologie, Universitat Bonn, Bonn, Deutschland
    Nervenarzt 81:807-8, 810-4. 2010
  8. ncbi Noradrenergic depletion increases inflammatory responses in brain: effects on IkappaB and HSP70 expression
    Michael T Heneka
    Department of Neurology, University of Bonn, Germany
    J Neurochem 85:387-98. 2003
  9. ncbi Neuroinflammatory processes in Alzheimer's disease
    Michael T Heneka
    Department of Neurology, Clinical Neurosciences, University of Bonn, Sigmund Freud Str 25, 53127 Bonn, Germany
    J Neural Transm 117:919-47. 2010
  10. pmc Locus ceruleus controls Alzheimer's disease pathology by modulating microglial functions through norepinephrine
    Michael T Heneka
    Department of Neurology, Deutsches Zentrum für Neurodegenerative Erkrankungen, University of Bonn, 53105 Bonn, Germany
    Proc Natl Acad Sci U S A 107:6058-63. 2010

Detail Information

Publications72

  1. pmc Impact and Therapeutic Potential of PPARs in Alzheimer's Disease
    Michael T Heneka
    University of Bonn, Department of Neurology, Clinical Neurosciences Unit, Bonn, Germany
    Curr Neuropharmacol 9:643-50. 2011
    ..Several clinical trials already revealed promising results using PPARγ agonists, therefore PPARγ represents an attractive therapeutic target for the treatment of AD...
  2. pmc Clinical symptoms and risk factors in cerebral microangiopathy patients
    Sandra Okroglic
    Department of Neurology, Clinical Neuroscience Unit, University of Bonn, Bonn, Germany
    PLoS ONE 8:e53455. 2013
    ..Hence, patterns of association among lesion topography and severity, clinical symptoms and demographic and disease risk factors were investigated retrospectively in a cohort of CM patients...
  3. pmc NLRP3 is activated in Alzheimer's disease and contributes to pathology in APP/PS1 mice
    Michael T Heneka
    Clinical Neuroscience Unit, Department of Neurology, University of Bonn, Sigmund Freud Strasse 25, 53127 Bonn, Germany
    Nature 493:674-8. 2013
    ..These results show an important role for the NLRP3/caspase-1 axis in the pathogenesis of Alzheimer's disease, and suggest that NLRP3 inflammasome inhibition represents a new therapeutic intervention for the disease...
  4. pmc Effect of anti-inflammatory agents on transforming growth factor beta over-expressing mouse brains: a model revised
    Pierre Lacombe
    Laboratoire de Recherches C r brovasculaires, CNRS FRE 2363, Paris, France
    J Neuroinflammation 1:11. 2004
    ..Identification of the thioflavin-S-positive material will facilitate the full appraisal of the clinical implication of the effects of anti-inflammatory drugs, and provide a more thorough understanding of TGF-beta1 actions in brain...
  5. pmc Norepinephrine enhances the LPS-induced expression of COX-2 and secretion of PGE2 in primary rat microglia
    Johannes C M Schlachetzki
    Department of Psychiatry and Psychotherapy, University Hospital of Freiburg, Freiburg, Germany
    J Neuroinflammation 7:2. 2010
    ..In the present study, we investigate the role of norepinephrine on cyclooxygenase- (COX-)2 expression/synthesis and prostaglandin (PG)E2 production in rat primary microglia...
  6. ncbi Molecular mechanisms and therapeutic application of NSAIDs and derived compounds in Alzheimer's disease
    M T Heneka
    Department of Neurology, Clinical Neurosciences, Unversity of Bonn, Sigmund Freud Str 25, 53127 Bonn, Germany
    Curr Alzheimer Res 8:115-31. 2011
    ..This article reviews the current knowledge and views on the above mechanisms and critically discusses current obstacles and the potential as future AD therapeutics...
  7. ncbi [Course modifying therapy of Alzheimer's dementia]
    M T Heneka
    Klinische Neurowissenschaften, Klinik und Poliklinik fur Neurologie, Universitat Bonn, Bonn, Deutschland
    Nervenarzt 81:807-8, 810-4. 2010
    ..Thus, the therapy of risk factors including arterial hypertension and obesity in midlife as well as a Mediterranean diet currently provides the highest chance of modifying the course of the disease...
  8. ncbi Noradrenergic depletion increases inflammatory responses in brain: effects on IkappaB and HSP70 expression
    Michael T Heneka
    Department of Neurology, University of Bonn, Germany
    J Neurochem 85:387-98. 2003
    ..These findings suggest one mechanism by which PPARgamma agonists could provide benefit in neurological diseases having an inflammatory component...
  9. ncbi Neuroinflammatory processes in Alzheimer's disease
    Michael T Heneka
    Department of Neurology, Clinical Neurosciences, University of Bonn, Sigmund Freud Str 25, 53127 Bonn, Germany
    J Neural Transm 117:919-47. 2010
    ....
  10. pmc Locus ceruleus controls Alzheimer's disease pathology by modulating microglial functions through norepinephrine
    Michael T Heneka
    Department of Neurology, Deutsches Zentrum für Neurodegenerative Erkrankungen, University of Bonn, 53105 Bonn, Germany
    Proc Natl Acad Sci U S A 107:6058-63. 2010
    ..Consequently, therapies targeting microglial phagocytosis should be tested under NE depletion...
  11. doi Neuroglia in neurodegeneration
    Michael T Heneka
    Klinische Neurowissenschaften, Klinik und Poliklinik fur Neurologie, 53127 Bonn, Germany
    Brain Res Rev 63:189-211. 2010
    ..The complex of recently acquired knowledge allows us to regard the neurodegenerative diseases as primarily gliodegenerative processes, in which glial cells determine the progression and outcome of neuropathological process...
  12. ncbi Acute treatment with the PPARgamma agonist pioglitazone and ibuprofen reduces glial inflammation and Abeta1-42 levels in APPV717I transgenic mice
    Michael T Heneka
    Department of Neurology, University of Bonn, Bonn, Germany
    Brain 128:1442-53. 2005
    ..These findings demonstrate that anti-inflammatory drugs can act rapidly to inhibit inflammatory responses in the brain and negatively modulate amyloidogenesis...
  13. doi NOS2 gene deficiency protects from sepsis-induced long-term cognitive deficits
    Marc Weberpals
    Department of Neurology, University of Bonn, 53127 Bonn, Germany
    J Neurosci 29:14177-84. 2009
    ..Together, this data set outlines the importance of the NOS2 activation for long-term cerebral changes after severe sepsis...
  14. pmc Nonsteroidal anti-inflammatory drugs repress beta-secretase gene promoter activity by the activation of PPARgamma
    Magdalena Sastre
    Department of Neurology, University of Bonn, Sigmund Freud Strasse 25, 53127 Bonn, Germany
    Proc Natl Acad Sci U S A 103:443-8. 2006
    ....
  15. doi Nitration of tyrosine 10 critically enhances amyloid β aggregation and plaque formation
    Markus P Kummer
    Clinical Neuroscience Unit, Department of Neurology, University of Bonn, Sigmund Freud Strasse 25, 53127 Bonn, Germany
    Neuron 71:833-44. 2011
    ..Further, injection of 3NTyr(10)-Aβ into the brain of young APP/PS1 mice induced β-amyloidosis. This suggests a disease modifying role for NOS2 in AD and therefore represents a potential therapeutic target...
  16. pmc Sepsis causes neuroinflammation and concomitant decrease of cerebral metabolism
    Alexander Semmler
    Department of Neurology, University Bonn, Bonn, Germany
    J Neuroinflammation 5:38. 2008
    ..Changes in cerebral blood flow, release of inflammatory molecules and metabolic alterations contribute to neuronal dysfunction and cell death...
  17. ncbi Noradrenergic depletion potentiates beta -amyloid-induced cortical inflammation: implications for Alzheimer's disease
    Michael T Heneka
    Department of Neurology, University of Bonn, Germany 53127
    J Neurosci 22:2434-42. 2002
    ..These data demonstrate that LC loss and NE depletion augment inflammatory responses to Abeta and suggest that LC loss in AD is permissive for increased inflammation and neuronal cell death...
  18. ncbi Locus ceruleus degeneration promotes Alzheimer pathogenesis in amyloid precursor protein 23 transgenic mice
    Michael T Heneka
    Department of Neurology, University of Bonn, 53127 Bonn, Germany
    J Neurosci 26:1343-54. 2006
    ..Our data demonstrate that the degeneration of LC affects morphology, metabolism, and function of amyloid plaque-containing higher brain regions in APP23 mice. We postulate that LC degeneration substantially contributes to AD development...
  19. ncbi Contribution of inflammatory processes to Alzheimer's disease: molecular mechanisms
    Magdalena Sastre
    Department of Neurology, University of Bonn, Sigmund Freud Str 25, 53127 Bonn, Germany
    Int J Dev Neurosci 24:167-76. 2006
    ..The implication of PPAR-gamma in the control of Abeta-induced inflammation suggests a new target for AD therapy and emphasize the contribution of neuroinflammatory mechanisms to the pathogenesis of AD...
  20. doi Persistent cognitive impairment, hippocampal atrophy and EEG changes in sepsis survivors
    Alexander Semmler
    Department of Neurology, University of Bonn, Bonn, Germany
    J Neurol Neurosurg Psychiatry 84:62-9. 2013
    ....
  21. doi PPARγ/RXRα-induced and CD36-mediated microglial amyloid-β phagocytosis results in cognitive improvement in amyloid precursor protein/presenilin 1 mice
    Mitsugu Yamanaka
    Clinical Neuroscience Unit, Department of Neurology, University of Bonn Medical Center, 53127 Bonn, Germany
    J Neurosci 32:17321-31. 2012
    ..Furthermore, DSP-8658-treated mice showed improved spatial memory performance. Therefore, stimulation of microglial clearance by simultaneous activation of the PPARγ/RXRα heterodimer may prove beneficial in prevention of AD...
  22. ncbi Systemic inflammation induces apoptosis with variable vulnerability of different brain regions
    Alexander Semmler
    Department of Neurology, University of Bonn, Germany
    J Chem Neuroanat 30:144-57. 2005
    ..We therefore conclude, that peripheral inflammation leads to a profound glial activation, the generation of nitric oxide and changes of Bax and Bcl-2 protein regulation critical for apoptosis...
  23. ncbi Noradrenaline induces expression of peroxisome proliferator activated receptor gamma (PPARgamma) in murine primary astrocytes and neurons
    Luisa Klotz
    Department of Neurology, University of Bonn, Bonn, Germany
    J Neurochem 86:907-16. 2003
    ..Conversely, decreased NA due to LC cell death in AD may reduce endogenous PPARgamma expression and therefore potentiate neuroinflammatory processes...
  24. ncbi Anti-inflammatory and antiproliferative actions of PPAR-gamma agonists on T lymphocytes derived from MS patients
    Stephan Schmidt
    Department of Neurology, University of Bonn, Germany
    J Leukoc Biol 75:478-85. 2004
    ..In summary, the data support the potential use of PPAR-gamma agonists as immunomodulatory, therapeutic agents for autoimmune diseases...
  25. doi Selective loss of noradrenaline exacerbates early cognitive dysfunction and synaptic deficits in APP/PS1 mice
    Thea Hammerschmidt
    Department of Neurology, Clinical Neurosciences, University of Bonn, Bonn, Germany
    Biol Psychiatry 73:454-63. 2013
    ..Because the LC contains multiple neuromodulators known to affect amyloid β toxicity and cognitive function, the specific role of noradrenaline (NA) in AD is not well understood...
  26. ncbi Long-term cognitive impairment, neuronal loss and reduced cortical cholinergic innervation after recovery from sepsis in a rodent model
    Alexander Semmler
    Department of Neurology, Sigmund Freud Strasse 25, University Hospital Bonn, 53105 Bonn, Germany
    Exp Neurol 204:733-40. 2007
    ..Together these results suggest that sepsis can induce persistent behavioral and neuroanatomical changes and warrant studies of the neurological long-term consequences of sepsis in humans...
  27. doi Nitric oxide decreases the enzymatic activity of insulin degrading enzyme in APP/PS1 mice
    Markus P Kummer
    Clinical Neurosciences Unit, Department of Neurology, University of Bonn, Sigmund Freud Strasse 25, 53105 Bonn, Germany
    J Neuroimmune Pharmacol 7:165-72. 2012
    ..These data suggest that NOS2 upregulation impairs amyloid β degradation through negative regulation of IDE activity and thus loss of NOS2 activity will positively influence amyloid β clearance...
  28. ncbi Proinflammatory stimulation and pioglitazone treatment regulate peroxisome proliferator-activated receptor gamma levels in peripheral blood mononuclear cells from healthy controls and multiple sclerosis patients
    Luisa Klotz
    Department of Neurology, University of Bonn, Germany
    J Immunol 175:4948-55. 2005
    ....
  29. ncbi Nonsteroidal anti-inflammatory drugs and peroxisome proliferator-activated receptor-gamma agonists modulate immunostimulated processing of amyloid precursor protein through regulation of beta-secretase
    Magdalena Sastre
    Department of Neurology, University of Bonn, 53127 Bonn, Germany
    J Neurosci 23:9796-804. 2003
    ..In conclusion, proinflammatory cytokines activate beta-secretase, and NSAIDs inhibit this effect through PPARgamma...
  30. doi Restraint stress increases neuroinflammation independently of amyloid β levels in amyloid precursor protein/PS1 transgenic mice
    Beatriz G Perez Nievas
    Department of Neurology, Clinical Neuroscience Unit, University of Bonn Medical Center, Bonn, Germany
    J Neurochem 116:43-52. 2011
    ..Since inflammation may act as a factor that contributes disease progression, the stress-inflammation relation described here may be relevant to understand the initial mechanisms in underlying the risk enhancing action of stress on AD...
  31. pmc CNS-targeted production of IL-17A induces glial activation, microvascular pathology and enhances the neuroinflammatory response to systemic endotoxemia
    Julian Zimmermann
    Department of Neurology, Universitatsklinikum Bonn, Bonn, Germany
    PLoS ONE 8:e57307. 2013
    ..More likely IL-17A acts as a modulating factor in the network of induced cytokines. This novel mouse model will be a very useful tool to further characterize the role of IL-17A in neuroinflammatory disease models...
  32. doi Mrp14 deficiency ameliorates amyloid β burden by increasing microglial phagocytosis and modulation of amyloid precursor protein processing
    Markus P Kummer
    Clinical Neurosciences Unit, Department of Neurology, University of Bonn, 53105 Bonn, Germany
    J Neurosci 32:17824-9. 2012
    ..We therefore conclude that Mrp14 promotes APP processing and Aβ accumulation under neuroinflammatory conditions...
  33. doi Locus coeruleus degeneration exacerbates olfactory deficits in APP/PS1 transgenic mice
    Nolwen L Rey
    Laboratoire Neurosciences Sensorielles, Comportement, Cognition, UMR5020 CNRS, University Lyon1, University of Lyon, Lyon, France
    Neurobiol Aging 33:426.e1-11. 2012
    ..Importantly, DSP4 treatment also increased amyloid β (Aβ) deposition in the olfactory bulb of APP/PS1 mice, which correlated with olfactory memory, not with discrimination deficits...
  34. doi Neuroinflammatory and behavioural changes in the Atp7B mutant mouse model of Wilson's disease
    Dick Terwel
    Department of Neurology, Clinical Neurosciences, Bonn University, Bonn, Germany
    J Neurochem 118:105-12. 2011
    ..These mice can be used to evaluate therapeutic strategies to alleviate behavioural disturbances and cerebral pathology observed in WD...
  35. doi Critical role of astroglial apolipoprotein E and liver X receptor-α expression for microglial Aβ phagocytosis
    Dick Terwel
    Department of Neurology, University of Bonn, 53127 Bonn, Germany
    J Neurosci 31:7049-59. 2011
    ..Together, these data suggest that astrocytic LXRα activation and subsequent release of ApoE by astrocytes is critical for the ability of microglia to remove fibrillar Aβ in response to treatment with TO901317...
  36. ncbi The oral antidiabetic pioglitazone protects from neurodegeneration and amyotrophic lateral sclerosis-like symptoms in superoxide dismutase-G93A transgenic mice
    Burkhard Schütz
    Department of Psychiatry and Psychotherapy, University of Bonn, 53127 Bonn, Germany
    J Neurosci 25:7805-12. 2005
    ..Interestingly, mRNA levels of the suppressor of cytokine signaling 1 and 3 genes were increased by Pio, whereas both the mRNA and protein levels of endogenous mouse SOD1 and of transgenic human SOD1 remained unaffected...
  37. ncbi Inflammatory processes in Alzheimer's disease
    Michael T Heneka
    Department of Neurology, Molecular Neurology Unit, University of Munster, Mendelstrasse 7, D 48149, Munster, Germany
    J Neuroimmunol 184:69-91. 2007
    ....
  38. ncbi GGA1 is expressed in the human brain and affects the generation of amyloid beta-peptide
    Tina Wahle
    Department of Neurology, University of Bonn, 53127 Bonn, Germany
    J Neurosci 26:12838-46. 2006
    ..Thus, GGA proteins might be involved in the pathogenesis of AD...
  39. pmc Ear2 deletion causes early memory and learning deficits in APP/PS1 mice
    Markus P Kummer
    Department of Neurology, Clinical Neurosciences Unit, University of Bonn, 53127 Bonn, Germany
    J Neurosci 34:8845-54. 2014
    ..Thus, early LC degeneration and subsequent NA reduction may contribute to cognitive deficits via CaMKII and NMDA receptor dysfunction independent of Aβ and suggests that NA supplementation could be beneficial in treating AD...
  40. pmc Focal glial activation coincides with increased BACE1 activation and precedes amyloid plaque deposition in APP[V717I] transgenic mice
    Michael T Heneka
    Department of Neurology, University of Munster, 48149 Munster, Germany
    J Neuroinflammation 2:22. 2005
    ..Transgenic mice overexpressing the london mutant of amyloid precursor protein, APP [V717I], robustly recapitulate the amyloid pathology of AD...
  41. ncbi IFN-beta1a (Rebif) modifies the expression of microfilament-associated cell-cell contacts in C6 glioma cells
    Michael Harzheim
    Department of Neurology, University of Bonn, Sigmund Freud Strasse 25, D 53105 Bonn, Germany
    J Interferon Cytokine Res 23:83-9. 2003
    ..This effect may also contribute to the therapeutic action of IFN-beta1a in MS...
  42. pmc Statins promote the degradation of extracellular amyloid {beta}-peptide by microglia via stimulation of exosome-associated insulin-degrading enzyme (IDE) secretion
    Irfan Y Tamboli
    Departments of Neurology, University of Bonn, Sigmund Freud Strasse 25, 53127 Bonn, Germany
    J Biol Chem 285:37405-14. 2010
    ..These data demonstrate a novel pathway for the nonconventional secretion of IDE via exosomes. The modulation of this pathway could provide a new strategy to enhance the extracellular clearance of Aβ...
  43. pmc Extracellular phosphorylation of the amyloid β-peptide promotes formation of toxic aggregates during the pathogenesis of Alzheimer's disease
    Sathish Kumar
    Department of Neurology, University of Bonn, Bonn, Germany
    EMBO J 30:2255-65. 2011
    ..Phosphorylation of Aβ could represent an important molecular mechanism in the pathogenesis of the most common sporadic form of AD...
  44. ncbi Drug insight: effects mediated by peroxisome proliferator-activated receptor-gamma in CNS disorders
    Michael T Heneka
    Department of Neurology, University of Munster, Germany
    Nat Clin Pract Neurol 3:496-504. 2007
    ..The verification of these findings in human cells prompted the initiation of clinical studies evaluating PPARgamma activation in patients with multiple sclerosis...
  45. ncbi Induction of apoptosis in human and rat glioma by agonists of the nuclear receptor PPARgamma
    Thomas Zander
    Department of Neurology, University Bonn, Germany
    J Neurochem 81:1052-60. 2002
    ..Taken together, treatment of glioma cells with PPARgamma agonists may hold therapeutic potential for the treatment of gliomas...
  46. ncbi TLR2 is a primary receptor for Alzheimer's amyloid β peptide to trigger neuroinflammatory activation
    Shirong Liu
    Department of Neurology, University of the Saarland, 66421 Homburg Saar, Germany
    J Immunol 188:1098-107. 2012
    ..Our study demonstrated that TLR2 is a primary receptor for Aβ to trigger neuroinflammatory activation and suggested that inhibition of TLR2 in microglia could be beneficial in Alzheimer's disease pathogenesis...
  47. pmc Distinct modulation of microglial amyloid β phagocytosis and migration by neuropeptides (i)
    Sigal Fleisher-Berkovich
    Division of Clinical Neurosciences, Dept of Neurology, University of Bonn Medical Center, Bonn, Germany
    J Neuroinflammation 7:61. 2010
    ..These results suggest that neuropeptides play an important role in chemotaxis and Aβ clearance and modulate the brain's response to neuroinflammatory processes...
  48. ncbi Loss of gamma-secretase function impairs endocytosis of lipoprotein particles and membrane cholesterol homeostasis
    Irfan Y Tamboli
    Department of Neurology, University of Bonn, 53127 Bonn, Germany
    J Neurosci 28:12097-106. 2008
    ..Thus, these data demonstrate a functional link between two major genetic factors that cause early-onset and late-onset Alzheimer's disease...
  49. pmc CXCR3 modulates glial accumulation and activation in cuprizone-induced demyelination of the central nervous system
    Marius Krauthausen
    Department of Neurology, Universitatsklinikum Bonn, Sigmund Freud Str, 25, D 53105 Bonn, Germany
    J Neuroinflammation 11:109. 2014
    ....
  50. pmc Opposing roles for CXCR3 signaling in central nervous system versus ocular inflammation mediated by the astrocyte-targeted production of IL-12
    Marius Krauthausen
    Department of Neurology, Universitatsklinikum Bonn, Bonn, Germany
    Am J Pathol 179:2346-59. 2011
    ..We conclude that the function of CXCR3 in cellular immune disease is driven by a common trigger and is controlled by tissue-specific factors...
  51. ncbi Long-term cerebral consequences of sepsis
    Catherine N Widmann
    Department of Neurology, Clinical Neuroscience Unit, University of Bonn, Bonn, Germany German Centre for Neurodegenerative Diseases, Bonn, Germany
    Lancet Neurol 13:630-6. 2014
    ..Key opportunities for neuroprotective interventions and after-care for people who have survived sepsis might be lost because the long-term neurocognitive and functional consequences of sepsis are not fully characterised. ..
  52. doi Studying M1 and M2 states in adult microglia
    Sadanand M Gaikwad
    University of Bonn, Bonn, Germany
    Methods Mol Biol 1041:185-97. 2013
    ..Likewise, adult microglia generated by this protocol can be used for functional analysis through cell cultivation for a limited time. ..
  53. ncbi PPARs in the brain
    Michael T Heneka
    Department of Neurology, Molecular Neurology Unit, Mendelstrasse 7, University of Munster, Albert Schweitzer Strasse 33, 48149 Munster, Germany
    Biochim Biophys Acta 1771:1031-45. 2007
    ..Less is known about the physiological role of PPARs for brain development, maintenance and function. Lesions from transgenic mouse models, however, provide evidence that PPARs may play pivotal roles for CNS development and function...
  54. ncbi Innate immune activation in neurodegenerative disease
    Michael T Heneka
    1 Clinical Neuroscience, Department of Neurology, University of Bonn, Sigmund Freud Strasse 25, 53127 Bonn, Germany 2 Department of Internal Medicine, University of Massachusetts, Worcester, Massachusetts 01605, USA 3 German Center for Neurodegenerative Diseases DZNE, Ludwig Erhard Allee 2, 53175 Bonn, Germany
    Nat Rev Immunol 14:463-77. 2014
    ..As chronic neuroinflammation is observed at relatively early stages of neurodegenerative disease, targeting the mechanisms that drive this process may be useful for diagnostic and therapeutic purposes. ..
  55. pmc Cerebral haemodynamics and carbon dioxide reactivity during sepsis syndrome
    Christof Thees
    Department of Anaesthesiology and Intensive Care Medicine, University of Bonn, 53105 Bonn, Germany
    Crit Care 11:R123. 2007
    ..We hypothesized that cerebral haemodynamics and carbon dioxide reactivity would be impaired in patients with sepsis syndrome and pathological electroencephalogram patterns...
  56. ncbi Glucose metabolism, gray matter structure, and memory decline in subjective memory impairment
    Lukas Scheef
    Department of Radiology, University of Bonn, Bonn, Germany
    Neurology 79:1332-9. 2012
    ..To identify biological evidence for Alzheimer disease (AD) in individuals with subjective memory impairment (SMI) and unimpaired cognitive performance and to investigate the longitudinal cognitive course in these subjects...
  57. pmc PPARs in Alzheimer's Disease
    Markus P Kummer
    Department of Neurology, University of Bonn, Sigmund Freud Strasse 25, 53127 Bonn, Germany
    PPAR Res 2008:403896. 2008
    ..Several clinical trials already revealed promising results using PPAR agonists, therefore PPARs represent an attractive therapeutic target for the treatment of AD...
  58. ncbi Peroxisome proliferator-activated receptor-gamma agonists prevent experimental autoimmune encephalomyelitis
    Douglas L Feinstein
    Department of Anesthesiology, University of Illinois, 11819 West Polk Street, MC519, Chicago, IL 60612, USA
    Ann Neurol 51:694-702. 2002
    ..Pioglitazone also reduced the antigen-dependent interferon-gamma production from EAE-derived T cells. These results suggest that orally administered PPARgamma agonists could provide therapeutic benefit in demyelinating disease...
  59. ncbi Beta-amyloid peptides decrease soluble guanylyl cyclase expression in astroglial cells
    Maria Antonia Baltrons
    Instituto de Biotecnología y Biomedicina V Villar Palasi, Departamento de Bioquímica Biologia Molecular, Universidad Autonoma de Barcelona, 08193, Bellaterra, Spain
    Neurobiol Dis 10:139-49. 2002
    ..A loss of sGC in reactive astrocytes surrounding beta-amyloid plaques could be a mechanism to prevent excess signalling via cGMP at sites of high NO production...
  60. ncbi Norepinephrine increases I kappa B alpha expression in astrocytes
    Vitaliy Gavrilyuk
    Department of Anesthesiology, University of Illinois at Chicago, Chicago, Illinois 60612, USA
    J Biol Chem 277:29662-8. 2002
    ..These results demonstrate that I kappa B alpha expression is regulated by NE at both transcriptional and post-transcriptional levels, which could contribute to the observed anti-inflammatory properties of NE in vitro and in vivo...
  61. ncbi Noradrenaline deficiency in brain increases beta-amyloid plaque burden in an animal model of Alzheimer's disease
    Sergey Kalinin
    Department of Anesthesiology, University of Illinois, and Jesse Brown Veteran s Affairs Research Division, Chicago, IL 60612, United States
    Neurobiol Aging 28:1206-14. 2007
    ..These findings suggest that noradrenergic innervation from LC are needed to maintain adequate Abeta clearance, and therefore that LC degeneration could contribute to AD pathogenesis...
  62. ncbi Antineoplastic effects of peroxisome proliferator-activated receptor gamma agonists
    Christian Grommes
    Department of Neurosciences, Alzheimer Research Laboratory, School of Medicine, Case Western Reserve University, Cleveland, OH, USA
    Lancet Oncol 5:419-29. 2004
    ..Here, we review PPAR gamma-induced antineoplastic signalling pathways, and summarise the antineoplastic effects of PPAR gamma agonists in different cancer cell lines, animal models, and clinical trials...
  63. pmc Reduction of amyloid angiopathy and Abeta plaque burden after enriched housing in TgCRND8 mice: involvement of multiple pathways
    Oliver Ambrée
    University Hospital Munster, Institute of Neuropathology, Domagkstr 19, D 48149, Munster, Germany
    Am J Pathol 169:544-52. 2006
    ..In summary, this study demonstrates that the environment interacts with AD pathology at dif-ferent levels...
  64. ncbi Inhibition of in vivo glioma growth and invasion by peroxisome proliferator-activated receptor gamma agonist treatment
    Christian Grommes
    Department of Neurosciences, Alzheimer Research Laboratory, Case Western Reserve University, Cleveland, Ohio, USA
    Mol Pharmacol 70:1524-33. 2006
    ..Together, these data indicate that pioglitazone may be of potential use in treatment of malignant gliomas...
  65. ncbi Suppressive effects of ansamycins on inducible nitric oxide synthase expression and the development of experimental autoimmune encephalomyelitis
    Patricia Murphy
    Department of Anesthesiology, University of Illinois, 1819 West Polk Street, Chicago, IL 60612, USA
    J Neurosci Res 67:461-70. 2002
    ..These results indicate that ansamycins can exert potent anti-inflammatory effects on brain glial cells which may provide therapeutic benefit in neuroinflammatory diseases...
  66. ncbi The nonthiazolidinedione tyrosine-based peroxisome proliferator-activated receptor gamma ligand GW7845 induces apoptosis and limits migration and invasion of rat and human glioma cells
    Christian Grommes
    Department of Neurosciences, Alzheimer Research Laboratory, Case Western Reserve University, Cleveland, Ohio, USA
    J Pharmacol Exp Ther 313:806-13. 2005
    ..There was also a reduction of migration and invasion, assessed by Boyden chamber and spheroid experiments. Together, these data indicate that the PPARgamma agonist GW7845 may be of potential use in treatment of malignant gliomas...
  67. ncbi Protection by pioglitazone in the MPTP model of Parkinson's disease correlates with I kappa B alpha induction and block of NF kappa B and iNOS activation
    Thomas Dehmer
    Neurodegeneration Laboratory, Center of Neurology and Hertie Institute for Clinical Brain Research, University of Tubingen, Tubingen, Germany
    J Neurochem 88:494-501. 2004
    ..In conclusion, treatment with pioglitazone may offer a treatment opportunity in PD to slow the progression of disease that is mediated by inflammation...
  68. ncbi Interleukin-1 beta and lipopolysaccharide decrease soluble guanylyl cyclase in brain cells: NO-independent destabilization of protein and NO-dependent decrease of mRNA
    Carlos E Pedraza
    Institute of Biotechnology and Biomedicine V Villar Palasi, and Department of Biochemistry and Molecular Biology, Autonomous University of Barcelona, 08193 Bellaterra, Spain
    J Neuroimmunol 144:80-90. 2003
    ..Additionally, both agents induce a NO-dependent decrease of sGC subunit mRNA. Decreased sGC subunit protein and mRNA levels are also observed in adult rat brain after focal injection of IL-1beta or LPS...
  69. ncbi Intrinsic regulation of brain inflammatory responses
    Elena Galea
    Department of Anesthesiology, University of Illinois, Chicago, Illinois, USA
    Cell Mol Neurobiol 23:625-35. 2003
    ....
  70. ncbi Multitracer positron emission tomographic imaging of exogenous gene expression mediated by a universal herpes simplex virus 1 amplicon vector
    Christiane Kummer
    Laboratory for Gene Therapy and Molecualr Imaging, Max Planck Institute for Neurological Research, Center for Molecualr Medicine, and Department of Neurology, University of Cologne, Cologne, Germany
    Mol Imaging 6:181-92. 2007
    ..The d2r80A in combination with a specific binding compound passing the intact blood-brain barrier might be an alternative marker gene for the noninvasive assessment of vector-mediated gene expression in the brain using PET...
  71. ncbi Imaging-guided gene therapy of experimental gliomas
    Andreas H Jacobs
    Laboratory for Gene Therapy and Molecular Imaging at the Max Planck Institute for Neurological Research, University of Cologne, Gleuelerstrasse 50, 50931 Cologne, Germany
    Cancer Res 67:1706-15. 2007
    ..This strategy will help in the development of safe and efficient gene therapy protocols for clinical application...
  72. ncbi Noradrenergic regulation of inflammatory gene expression in brain
    Douglas L Feinstein
    Department of Anesthesiology, University of Illinois, Chicago, IL, USA
    Neurochem Int 41:357-65. 2002
    ....