Mathias Jucker

Summary

Country: Germany

Publications

  1. doi request reprint Self-propagation of pathogenic protein aggregates in neurodegenerative diseases
    Mathias Jucker
    Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, D 72076 Tubingen, Germany
    Nature 501:45-51. 2013
  2. pmc Cerebral and peripheral amyloid phagocytes--an old liaison with a new twist
    Mathias Jucker
    Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, D 72076 Tubingen, Germany
    Neuron 59:8-10. 2008
  3. doi request reprint The benefits and limitations of animal models for translational research in neurodegenerative diseases
    Mathias Jucker
    Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Tubingen, Germany
    Nat Med 16:1210-4. 2010
  4. pmc Pathogenic protein seeding in Alzheimer disease and other neurodegenerative disorders
    Mathias Jucker
    Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Tubingen, Germany
    Ann Neurol 70:532-40. 2011
  5. pmc Independent effects of intra- and extracellular Abeta on learning-related gene expression
    Bettina 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
  6. pmc Peripherally applied Abeta-containing inoculates induce cerebral beta-amyloidosis
    Yvonne S Eisele
    Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, D 72076 Tubingen, Germany
    Science 330:980-2. 2010
  7. pmc Induction of cerebral beta-amyloidosis: intracerebral versus systemic Abeta inoculation
    Yvonne 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
  8. pmc E22Q-mutant Abeta peptide (AbetaDutch) increases vascular but reduces parenchymal Abeta deposition
    Martin 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
  9. doi request reprint Formation and maintenance of Alzheimer's disease beta-amyloid plaques in the absence of microglia
    Stefan A Grathwohl
    Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Tubingen, Germany
    Nat Neurosci 12:1361-3. 2009
  10. pmc 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

Collaborators

Detail Information

Publications54

  1. doi request reprint Self-propagation of pathogenic protein aggregates in neurodegenerative diseases
    Mathias Jucker
    Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, D 72076 Tubingen, Germany
    Nature 501:45-51. 2013
    ..As a unifying pathogenic principle, the prion paradigm suggests broadly relevant therapeutic directions for a large class of currently intractable diseases. ..
  2. pmc Cerebral and peripheral amyloid phagocytes--an old liaison with a new twist
    Mathias 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...
  3. doi request reprint The benefits and limitations of animal models for translational research in neurodegenerative diseases
    Mathias 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...
  4. pmc Pathogenic protein seeding in Alzheimer disease and other neurodegenerative disorders
    Mathias Jucker
    Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Tubingen, Germany
    Ann Neurol 70:532-40. 2011
    ....
  5. pmc Independent effects of intra- and extracellular Abeta on learning-related gene expression
    Bettina 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...
  6. pmc Peripherally applied Abeta-containing inoculates induce cerebral beta-amyloidosis
    Yvonne 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...
  7. pmc Induction of cerebral beta-amyloidosis: intracerebral versus systemic Abeta inoculation
    Yvonne 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
    ....
  8. pmc E22Q-mutant Abeta peptide (AbetaDutch) increases vascular but reduces parenchymal Abeta deposition
    Martin 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...
  9. doi request reprint Formation and maintenance of Alzheimer's disease beta-amyloid plaques in the absence of microglia
    Stefan 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...
  10. pmc 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...
  11. doi request reprint Long-term in vivo imaging of β-amyloid plaque appearance and growth in a mouse model of cerebral β-amyloidosis
    Jasmin 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...
  12. pmc Seeded strain-like transmission of β-amyloid morphotypes in APP transgenic mice
    Götz Heilbronner
    1 Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, D 72076 Tubingen, Germany 2 DZNE, German Center for Neurodegenerative Diseases, D 72076 Tubingen, Germany
    EMBO Rep 14:1017-22. 2013
    ..These results indicate that the molecular composition and conformation of aggregated Aβ in APP transgenic mice can be maintained by seeded conversion. ..
  13. pmc Microglial repopulation model reveals a robust homeostatic process for replacing CNS myeloid cells
    Nicholas 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
    ....
  14. doi request reprint Repeatable target localization for long-term in vivo imaging of mice with 2-photon microscopy
    Jasmin 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...
  15. ncbi request reprint Cystatin C modulates cerebral beta-amyloidosis
    Stephan 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...
  16. pmc Abeta42-driven cerebral amyloidosis in transgenic mice reveals early and robust pathology
    Rebecca 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
    ....
  17. pmc Neurogenesis and alterations of neural stem cells in mouse models of cerebral amyloidosis
    Florian 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...
  18. ncbi request reprint Abeta is targeted to the vasculature in a mouse model of hereditary cerebral hemorrhage with amyloidosis
    Martin C Herzig
    Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, D 72076 Tubingen, Germany
    Nat Neurosci 7:954-60. 2004
    ....
  19. doi request reprint Membrane-anchored Aβ accelerates amyloid formation and exacerbates amyloid-associated toxicity in mice
    Amudha Nagarathinam
    Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, D 72076 Tubingen, Germany, Graduate School for Cellular and Molecular Neuroscience, University of Tubingen, D 72076 Tubingen, Germany, German Center for Neurodegenerative Diseases, D 72076 Tubingen, Germany, and Animal Health and Veterinary Laboratories Agency, Lasswade Laboratory, Penicuik EH26 0PZ, Midlothian, United Kingdom
    J Neurosci 33:19284-94. 2013
    ..These in vivo findings support the hypothesis that Aβ-membrane interactions play a pivotal role in early-onset AD as well as neuronal damage and provide evidence to study Aβ-membrane interactions as therapeutic targets. ..
  20. pmc Dynamics of the microglial/amyloid interaction indicate a role in plaque maintenance
    Tristan 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...
  21. pmc Soluble Aβ seeds are potent inducers of cerebral β-amyloid deposition
    Franziska 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...
  22. doi request reprint Spectral discrimination of cerebral amyloid lesions after peripheral application of luminescent conjugated oligothiophenes
    Bettina 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
    ....
  23. doi request reprint Early onset amyloid lesions lead to severe neuritic abnormalities and local, but not global neuron loss in APPPS1 transgenic mice
    Niels J Rupp
    Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany
    Neurobiol Aging 32:2324.e1-6. 2011
    ....
  24. ncbi request reprint BACE1 and mutated presenilin-1 differently modulate Abeta40 and Abeta42 levels and cerebral amyloidosis in APPDutch transgenic mice
    Martin 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...
  25. doi request reprint The value of incomplete mouse models of Alzheimer's disease
    Rebecca 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
    ....
  26. pmc Modeling familial Danish dementia in mice supports the concept of the amyloid hypothesis of Alzheimer's disease
    Janaky 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...
  27. pmc The presence of Aβ seeds, and not age per se, is critical to the initiation of Aβ deposition in the brain
    Tsuyoshi Hamaguchi
    Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, 72076, Tubingen, Germany
    Acta Neuropathol 123:31-7. 2012
    ....
  28. ncbi request reprint Mechanism of cerebral beta-amyloid angiopathy: murine and cellular models
    Martin C Herzig
    Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Germany
    Brain Pathol 16:40-54. 2006
    ....
  29. doi request reprint Homeostatic and injury-induced microglia behavior in the aging brain
    Jasmin K Hefendehl
    Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, D 72076, Tubingen, Germany
    Aging Cell 13:60-9. 2014
    ..These results provide novel insights into microglial behavior and indicate that microglial dysfunction in the aging brain may contribute to age-related cognitive decline and neurodegenerative diseases. ..
  30. pmc Gleevec increases levels of the amyloid precursor protein intracellular domain and of the amyloid-beta degrading enzyme neprilysin
    Yvonne 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...
  31. doi request reprint Changes in amyloid-β and Tau in the cerebrospinal fluid of transgenic mice overexpressing amyloid precursor protein
    Luis F Maia
    Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, D 72076 Tubingen, Germany
    Sci Transl Med 5:194re2. 2013
    ..These findings also suggest that APP transgenic mouse models may be useful in the search for new disease markers for AD. ..
  32. ncbi request reprint Invasion of hematopoietic cells into the brain of amyloid precursor protein transgenic mice
    Anna 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...
  33. pmc Induction of tau pathology by intracerebral infusion of amyloid-beta -containing brain extract and by amyloid-beta deposition in APP x Tau transgenic mice
    Tristan 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
    ....
  34. doi request reprint Replacement of osmotic minipumps to extend the intracerebral infusion time of compounds into the mouse brain
    Stefan A Grathwohl
    Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, Tubingen, Germany
    Biotechniques 55:75-8. 2013
    ..Experimental evaluation of Y-con pump replacement revealed no signs of tissue irritation or hydrocephalus and allowed extended controlled delivery of infusion agents in the brain. ..
  35. ncbi request reprint Exogenous induction of cerebral beta-amyloidogenesis is governed by agent and host
    Melanie Meyer-Luehmann
    Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tubingen, D 72076 Tubingen, 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...
  36. ncbi request reprint Neocortical synaptic bouton number is maintained despite robust amyloid deposition in APP23 transgenic mice
    Sonia 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...
  37. pmc Changes in extracellular space size and geometry in APP23 transgenic mice: a model of Alzheimer's disease
    Eva 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
    ....
  38. ncbi request reprint Restricted diffusion in the brain of transgenic mice with cerebral amyloidosis
    Thomas 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...
  39. ncbi request reprint Amyloid-associated neuron loss and gliogenesis in the neocortex of amyloid precursor protein transgenic mice
    Luca 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...
  40. ncbi request reprint Induction of brain-derived neurotrophic factor in plaque-associated glial cells of aged APP23 transgenic mice
    Guido 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...
  41. ncbi request reprint Extracellular amyloid formation and associated pathology in neural grafts
    Melanie Meyer-Luehmann
    Department of Neuropathology, Institute of Pathology, University of Basel, Schonbeinstrasse 40, 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...
  42. ncbi request reprint Thrombolysis induces cerebral hemorrhage in a mouse model of cerebral amyloid angiopathy
    David T Winkler
    Department of Neuropathology, Institute of Pathology, University Hospital Basel, Schonbeinstrasse 40, CH 4003 Basel, Switzerland
    Ann Neurol 51:790-3. 2002
    ....
  43. ncbi request reprint Cholinergic changes in the APP23 transgenic mouse model of cerebral amyloidosis
    Sonia 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...
  44. ncbi request reprint Insensitivity to Abeta42-lowering nonsteroidal anti-inflammatory drugs and gamma-secretase inhibitors is common among aggressive presenilin-1 mutations
    Eva Czirr
    Emmy Noether Research Group, Mainz, Germany
    J Biol Chem 282:24504-13. 2007
    ....
  45. ncbi request reprint Vessel ultrastructure in APP23 transgenic mice after passive anti-Abeta immunotherapy and subsequent intracerebral hemorrhage
    Guido 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...
  46. ncbi request reprint MDR1-P-Glycoprotein (ABCB1) Mediates Transport of Alzheimer's amyloid-beta peptides--implications for the mechanisms of Abeta clearance at the blood-brain barrier
    Diana 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...
  47. ncbi request reprint Impact of age and caloric restriction on neurogenesis in the dentate gyrus of C57BL/6 mice
    Luca Bondolfi
    Department of Neuropathology, Institute of Pathology, University of Basel, Schonbeinstrasse 40, 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...
  48. ncbi request reprint Synapse loss in cortex of agrin-deficient mice after genetic rescue of perinatal death
    Iwona 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...
  49. ncbi request reprint Comparison of commissural sprouting in the mouse and rat fascia dentata after entorhinal cortex lesion
    Domenico 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...
  50. ncbi request reprint Lesion-induced axonal sprouting in the central nervous system
    Thomas 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...
  51. ncbi request reprint Inducible proteopathies
    Lary C Walker
    Yerkes National Primate Research Center and Department of Neurology, Emory University, Atlanta, GA 30322, USA
    Trends Neurosci 29:438-43. 2006
    ....
  52. ncbi request reprint Modeling familial British dementia in transgenic mice
    Fiona 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...
  53. pmc Expression pattern of the transcription factor Olig2 in response to brain injuries: implications for neuronal repair
    Annalisa 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...
  54. ncbi request reprint Emerging prospects for the disease-modifying treatment of Alzheimer's disease
    Lary 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...