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Genomes and Genes | Mathias JuckerSummaryCountry: Germany Publications
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Publications
Cerebral and peripheral amyloid phagocytes--an old liaison with a new twistMathias Jucker
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, D 72076 Tubingen, Germany
Neuron 59:8-10. 2008..This observation intensifies the longstanding controversy of whether mononuclear cells such as macrophages and/or microglial cells are beneficial or detrimental in AD...- Pathogenic protein seeding in Alzheimer disease and other neurodegenerative disordersMathias Jucker
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Tubingen, Germany
Ann Neurol 70:532-40. 2011.... 
The benefits and limitations of animal models for translational research in neurodegenerative diseasesMathias Jucker
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Tubingen, Germany
Nat Med 16:1210-4. 2010..This commentary summarizes current models and highlights key questions we should be asking about animal models, as well as questions that cannot be answered with the current models...- Independent effects of intra- and extracellular Abeta on learning-related gene expressionBettina M Wegenast-Braun
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, Graduate School of Cellular and Molecular Neuroscience, University of Tubingen, Germany
Am J Pathol 175:271-82. 2009..These results provide evidence that two independent Abeta pathologies converge in their impact on cognitive function in Alzheimer's disease... - E22Q-mutant Abeta peptide (AbetaDutch) increases vascular but reduces parenchymal Abeta depositionMartin C Herzig
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Otfried Muller Strasse 27, D 72076 Tubingen, Germany
Am J Pathol 174:722-6. 2009..Our findings suggest that AbetaDutch1-40 inhibits parenchymal amyloidosis but exacerbates vascular amyloid, hence explaining the compartment-specific distribution of cerebral amyloid in HCHWA-D patients... - Peripherally applied Abeta-containing inoculates induce cerebral beta-amyloidosisYvonne S Eisele
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, D 72076 Tubingen, Germany
Science 330:980-2. 2010..We found that intraperitoneal inoculation with β-amyloid-rich extracts induced β-amyloidosis in the brains of β-amyloid precursor protein transgenic mice after prolonged incubation times... - Neurogenesis and alterations of neural stem cells in mouse models of cerebral amyloidosisFlorian V Ermini
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Tubingen, Germany
Am J Pathol 172:1520-8. 2008..Results provide evidence for a disruption of neural stem cell biology in an amyloidogenic environment and support findings that neurogenesis is differently affected among various transgenic mouse models of Alzheimer's disease... - Formation and maintenance of Alzheimer's disease beta-amyloid plaques in the absence of microgliaStefan A Grathwohl
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Tubingen, Germany
Nat Neurosci 12:1361-3. 2009..Neither amyloid plaque formation and maintenance nor amyloid-associated neuritic dystrophy depended on the presence of microglia... - BRI2 protein regulates β-amyloid degradation by increasing levels of secreted insulin-degrading enzyme (IDE)Ellen Kilger
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, D 72076 Tubingen, Germany
J Biol Chem 286:37446-57. 2011..Targeting the regulation of IDE may be a promising therapeutic approach to sporadic AD... - Induction of cerebral beta-amyloidosis: intracerebral versus systemic Abeta inoculationYvonne S Eisele
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, D 72076 Tubingen, Germany
Proc Natl Acad Sci U S A 106:12926-31. 2009.... - Long-term in vivo imaging of β-amyloid plaque appearance and growth in a mouse model of cerebral β-amyloidosisJasmin K Hefendehl
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Tubingen, Germany
J Neurosci 31:624-9. 2011..A solid knowledge of the dynamics of cerebral β-amyloidosis in mouse models provides a powerful tool to monitor preclinical Aβ targeting therapeutic strategies and eases the interpretation of diagnostic amyloid imaging in humans... - Microglial repopulation model reveals a robust homeostatic process for replacing CNS myeloid cellsNicholas H Varvel
German Center for Neurodegenerative Diseases, DZNE, and Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tuebingen, 72076 Tuebingen, Germany
Proc Natl Acad Sci U S A 109:18150-5. 2012.... - Repeatable target localization for long-term in vivo imaging of mice with 2-photon microscopyJasmin K Hefendehl
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, D 72076 Tubingen, Germany
J Neurosci Methods 205:357-63. 2012..Thus, here described head fixation device appears well suited for in vivo repetitive long-term imaging in rodent brain... - Modeling familial Danish dementia in mice supports the concept of the amyloid hypothesis of Alzheimer's diseaseJanaky Coomaraswamy
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, Graduate School of Cellular and Molecular Neuroscience, University of Tubingen, 72076 Tubingen, Germany
Proc Natl Acad Sci U S A 107:7969-74. 2010..Our results support the concept of the amyloid hypothesis for AD and related dementias, and suggest that different proteins prone to amyloid formation can drive strikingly similar pathogenic pathways in the brain... - Induction of tau pathology by intracerebral infusion of amyloid-beta -containing brain extract and by amyloid-beta deposition in APP x Tau transgenic miceTristan Bolmont
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Otfried Müller Str 27, D 72076 Tubingen, Germany
Am J Pathol 171:2012-20. 2007.... 
Cystatin C modulates cerebral beta-amyloidosisStephan A Kaeser
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Otfried Muller Strasse 27, D 72076 Tubingen, Germany
Nat Genet 39:1437-9. 2007..Our results suggest that cystatin C concentrations modulate cerebral amyloidosis risk and provide an opportunity for genetic risk assessment and therapeutic interventions...- Abeta42-driven cerebral amyloidosis in transgenic mice reveals early and robust pathologyRebecca Radde
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, Otfried Muller Strasse 27, D 72076 Tubingen, Germany
EMBO Rep 7:940-6. 2006.... - Dynamics of the microglial/amyloid interaction indicate a role in plaque maintenanceTristan Bolmont
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, D 72076 Tubingen, Germany
J Neurosci 28:4283-92. 2008..These results indicate a role for microglia in plaque maintenance and provide a model with multiple targets for therapeutic intervention... - Soluble Aβ seeds are potent inducers of cerebral β-amyloid depositionFranziska Langer
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, D 72076 Tubingen, Germany
J Neurosci 31:14488-95. 2011..If they can be identified in vivo, soluble Aβ seeds in bodily fluids also could serve as early biomarkers for cerebral β-amyloidogenesis and eventually Alzheimer's disease... - Abeta is targeted to the vasculature in a mouse model of hereditary cerebral hemorrhage with amyloidosisMartin C Herzig
Department of Cellular Neurology, Hertie-Institute for Clinical Brain Research, , , Germany
Nat Neurosci 7:954-60. 2004.... - Early onset amyloid lesions lead to severe neuritic abnormalities and local, but not global neuron loss in APPPS1 transgenic miceNiels J Rupp
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany
Neurobiol Aging 32:2324.e1-6. 2011.... - The value of incomplete mouse models of Alzheimer's diseaseRebecca Radde
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Otfried Muller Strasse 27, Tubingen, Germany
Eur J Nucl Med Mol Imaging 35:S70-4. 2008.... - BACE1 and mutated presenilin-1 differently modulate Abeta40 and Abeta42 levels and cerebral amyloidosis in APPDutch transgenic miceMartin C Herzig
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Tubingen, Germany
Neurodegener Dis 4:127-35. 2007..We conclude that the absolute levels of Abeta in combination with the ratio of Abeta42 to Abeta40 play a key role in determining the cerebral compartment and brain region in which Abeta is deposited... - The presence of Aβ seeds, and not age per se, is critical to the initiation of Aβ deposition in the brainTsuyoshi Hamaguchi
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, 72076, Tubingen, Germany
Acta Neuropathol 123:31-7. 2012.... - Mechanism of cerebral beta-amyloid angiopathy: murine and cellular modelsMartin C Herzig
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Germany
Brain Pathol 16:40-54. 2006.... - Gleevec increases levels of the amyloid precursor protein intracellular domain and of the amyloid-beta degrading enzyme neprilysinYvonne S Eisele
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, D 72076 Tubingen, Germany
Mol Biol Cell 18:3591-600. 2007..Thus, the Gleevec mediated-increase in neprilysin expression may involve enhanced AICD signaling. The finding that Gleevec elevates neprilysin levels suggests that its Abeta-lowering effect may be caused by increased Abeta-degradation... - Spectral discrimination of cerebral amyloid lesions after peripheral application of luminescent conjugated oligothiophenesBettina M Wegenast-Braun
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Otfried Mueller Strasse 2, Tubingen, Germany
Am J Pathol 181:1953-60. 2012.... - Invasion of hematopoietic cells into the brain of amyloid precursor protein transgenic miceAnna K Stalder
Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, D 72076 Tubingen, Germany
J Neurosci 25:11125-32. 2005..The observation that hematopoietic cells invade the brain in response to cerebral amyloidosis may hold an unrecognized therapeutic potential... - Exogenous induction of cerebral beta-amyloidogenesis is governed by agent and hostMelanie Meyer-Luehmann
Department of Cellular Neurology, Hertie-Institute for Clinical Brain Research, , , Germany
Science 313:1781-4. 2006..The phenotype of the exogenously induced amyloidosis depended on both the host and the source of the agent, suggesting the existence of polymorphic Abeta strains with varying biological activities reminiscent of prion strains... - Cholinergic changes in the APP23 transgenic mouse model of cerebral amyloidosisSonia Boncristiano
Neuropathology, Institute for Pathology, University of Basel, CH 4003 Basel, Switzerland
J Neurosci 22:3234-43. 2002..Moreover, our results suggest that disruption of the basal cholinergic forebrain system does not promote cerebral amyloidosis in APP23 transgenic mice... - Induction of brain-derived neurotrophic factor in plaque-associated glial cells of aged APP23 transgenic miceGuido J Burbach
Institute of Clinical Neuroanatomy, J. W. Goethe University, D-60590 Frankfurt, Germany
J Neurosci 24:2421-30. 2004..Taken together, our data demonstrate a plaque-associated upregulation of BDNF in APP23 transgenic mice and implicate this neurotrophin in the regulation of inflammatory and axonal growth processes in the plaque vicinity... - Restricted diffusion in the brain of transgenic mice with cerebral amyloidosisThomas Mueggler
Discovery Technologies, Novartis Institute for Biomedical Research, CH-4002 Basel, Switzerland
Eur J Neurosci 20:811-7. 2004..Reduced diffusivity within the interstitial space may alter volume transmission and therefore contribute to the cognitive impairment in Alzheimer's disease... - Insensitivity to Abeta42-lowering nonsteroidal anti-inflammatory drugs and gamma-secretase inhibitors is common among aggressive presenilin-1 mutationsEva Czirr
Emmy Noether Research Group, Mainz, Germany
J Biol Chem 282:24504-13. 2007.... - Changes in extracellular space size and geometry in APP23 transgenic mice: a model of Alzheimer's diseaseEva Sykova
Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Videnska 1083, 142 20 Prague 4, Czech Republic
Proc Natl Acad Sci U S A 102:479-84. 2005.... - Neocortical synaptic bouton number is maintained despite robust amyloid deposition in APP23 transgenic miceSonia Boncristiano
Department of Neuropathology, Institute of Pathology, University of Basel, Switzerland
Neurobiol Aging 26:607-13. 2005..Our results suggest that cerebral amyloidosis is not sufficient to account for the global synapse loss in AD. Alternatively, a putative trophic effect of APP may prevent, compensate, or delay a loss of synapses in this mouse model... - Amyloid-associated neuron loss and gliogenesis in the neocortex of amyloid precursor protein transgenic miceLuca Bondolfi
Department of Neuropathology, Institute of Pathology, University of Basel, CH 4003 Basel, Switzerland
J Neurosci 22:515-22. 2002..The majority were microglial and to a lesser extent astroglial cells. We conclude that cerebral amyloidosis in APP23 mice causes a modest neuron loss in neocortex and induces marked gliogenesis... - MDR1-P-Glycoprotein (ABCB1) Mediates Transport of Alzheimer's amyloid-beta peptides--implications for the mechanisms of Abeta clearance at the blood-brain barrierDiana Kuhnke
Department of Pharmacology, Research Center of Pharmacology and Experimental Therapeutics, Ernst Moritz Arndt University, Greifswald, Germany
Brain Pathol 17:347-53. 2007..Our data support the concept that P-gp is important for the clearance of Abeta from brain, and thus may represent a target protein for the prevention and/or treatment of neurodegenerative disorders such as AD... - Thrombolysis induces cerebral hemorrhage in a mouse model of cerebral amyloid angiopathyDavid T Winkler
Department of Neuropathology, Institute of Pathology, University Hospital Basel, , CH-4003 Basel, Switzerland
Ann Neurol 51:790-3. 2002.... - Vessel ultrastructure in APP23 transgenic mice after passive anti-Abeta immunotherapy and subsequent intracerebral hemorrhageGuido J Burbach
Institute of Clinical Neuroanatomy, J W Goethe University, Theodor Stern Kai 7, D 60590 Frankfurt, Germany
Neurobiol Aging 28:202-12. 2007..Minor structural alterations of the vessel wall, however, cannot be excluded due to the sample size of our study and the high complexity of the three-dimensional vessel wall ultrastructure... - Extracellular amyloid formation and associated pathology in neural graftsMelanie Meyer-Luehmann
Department of Neuropathology, Institute of Pathology, University of Basel, , CH-4003 Basel, Switzerland
Nat Neurosci 6:370-7. 2003..Our results indicate that diffusion of soluble Abeta in the extracellular space is involved in the spread of Abeta pathology, and that extracellular amyloid formation can lead to neurodegeneration... - Comparison of commissural sprouting in the mouse and rat fascia dentata after entorhinal cortex lesionDomenico Del Turco
Institute of Clinical Neuroanatomy, J. W. Goethe University, Frankfurt/Main, Germany
Hippocampus 13:685-99. 2003..These data demonstrate an important species difference in the commissural/associational sprouting response between rats and mice that needs to be taken into account in future studies... - Emerging prospects for the disease-modifying treatment of Alzheimer's diseaseLary C Walker
Yerkes National Primate Research Center, Emory University, 954 Gatewood Road, Atlanta, GA 30322, USA
Biochem Pharmacol 69:1001-8. 2005..These adverse events were not anticipated from preclinical studies with rodents; hence, more biologically relevant models, such as nonhuman primates, are needed to test the safety and efficacy of novel therapies for Alzheimer's disease... - Impact of age and caloric restriction on neurogenesis in the dentate gyrus of C57BL/6 miceLuca Bondolfi
Department of Neuropathology, Institute of Pathology, University of Basel, , CH-4003 Basel, Switzerland
Neurobiol Aging 25:333-40. 2004..Long-term CR does not counteract this age-related decline in neurogenesis but promotes survival of hilar glial cells... - Synapse loss in cortex of agrin-deficient mice after genetic rescue of perinatal deathIwona Ksiazek
Biozentrum, University of Basel, CH 4056 Basel, Switzerland
J Neurosci 27:7183-95. 2007..In summary, our results provide strong evidence that agrin plays an important role in the formation and/or the maintenance of excitatory synapses in the brain, and we provide evidence that this function involves MAP kinase signaling... - Expression pattern of the transcription factor Olig2 in response to brain injuries: implications for neuronal repairAnnalisa Buffo
Institute for Stem Cell Research, National Research Center for Environment and Health, Neuherberg Munich, Germany
Proc Natl Acad Sci U S A 102:18183-8. 2005..These data, therefore, imply Olig2 as a repressor of neurogenesis in cells reacting to brain injury and open innovative perspectives toward evoking endogenous neuronal repair... - Lesion-induced axonal sprouting in the central nervous systemThomas Deller
Institute of Clinical Neuroanatomy, Johann Wolfgang Goether-University, Frankfurt am Main, Germany
Adv Exp Med Biol 557:101-21. 2006..Finally, we discuss both the beneficial as well as disadvantageous functional implications of axonal sprouting for the injured organism in question... - Modeling familial British dementia in transgenic miceFiona Pickford
Department of Neuroscience, Mayo Clinic College of Medicine, Jacksonville, FL 92224, USA
Brain Pathol 16:80-5. 2006..This review discusses the strategies chosen and problems experienced with the development of FBD/FDD models and suggests novel approaches to model the diseases in murine models... - Inducible proteopathiesLary C Walker
Yerkes National Primate Research Center and Department of Neurology, Emory University, Atlanta, GA 30322, USA
Trends Neurosci 29:438-43. 2006....