- Neurotrophic factors in Alzheimer's disease: role of axonal transportK Schindowski
Institut National de la Santé et de la Research Médicale U837, Universite Lille 2, Lille Cedex, France
Genes Brain Behav 7:43-56. 2008....
- Increased T-cell reactivity and elevated levels of CD8+ memory T-cells in Alzheimer's disease-patients and T-cell hyporeactivity in an Alzheimer's disease-mouse model: implications for immunotherapyKatharina Schindowski
Institute of Pharmacology, Biocenter building N260, Johann Wolfgang Goethe University, Max von Laue Strasse 9, 60438 Frankfurt am Main, Germany
Neuromolecular Med 9:340-54. 2007..Our data implicate the generation of reactive memory T-cell in AD and of anergic memory T-cells in transgenic mice and should be taken into concern when designing immunotherapy...
- Apoptosis of CD4+ T and natural killer cells in Alzheimer's diseaseK Schindowski
Institute of Pharmacology, Biocenter, Johann Wolfgang Goethe University, Frankfurt, Germany
Pharmacopsychiatry 39:220-8. 2006..Immunotherapy appears to be a potent treatment against Alzheimer's disease (AD), but the mechanisms underlying neural-immune interaction are still not known...
- Alzheimer's disease-like tau neuropathology leads to memory deficits and loss of functional synapses in a novel mutated tau transgenic mouse without any motor deficitsKatharina Schindowski
INSERM U815, Place de Verdun, 59045 Lille Cedex, France
Am J Pathol 169:599-616. 2006..This model will serve as an experimental tool in future studies to investigate mechanisms underlying cognitive deficits during pathogenic tau aggregation...
- Age-related increase of oxidative stress-induced apoptosis in mice prevention by Ginkgo biloba extract (EGb761)K Schindowski
Department of Pharmacology, Biocenter, Johann Wolfgang Goethe University, Frankfurt am Main, Federal Republic of Germany
J Neural Transm 108:969-78. 2001..In addition, mice were treated daily with 100 mg/kg EGb761 per os over a period of two weeks. ROS-induced apoptosis was significantly reduced in the EGb761 group. Interestingly, this effect seemed to be more pronounced in old mice...
- Enhanced ROS-generation in lymphocytes from Alzheimer's patientsS Leutner
Department of Pharmacology, Biocenter, J W Goethe University of Frankfurt, Marie Curie Str 9, 60439 Frankfurt am Main, Germany
Pharmacopsychiatry 38:312-5. 2005..The objective of the present study was to evaluate whether the mechanisms involved in the generation of oxidative stress in normal senescence and Alzheimer's disease are identical or not...
- Age-related changes of apoptotic cell death in human lymphocytesK Schindowski
Institute of Pharmacology, Biocenter, Johann Wolfgang Goethe University, Frankfurt am Main, Germany
Neurobiol Aging 21:661-70. 2000..Expression of Bcl-2 was increased in aging and correlated with the number of apoptotic cells...
- Alzheimer's disease-like alterations in peripheral cells from presenilin-1 transgenic miceA Eckert
Department of Pharmacology, Biocenter, University of Frankfurt, Marie Curie Strasse 9, Frankfurt, D 60439, Germany
Neurobiol Dis 8:331-42. 2001....
- Neurogenesis and cell cycle-reactivated neuronal death during pathogenic tau aggregationK Schindowski
INSERM, U837, Place de Verdun, Lille Cedex, France
Genes Brain Behav 7:92-100. 2008..Altogether, these data suggest that cell cycle events in THY-Tau22 are resulting from neurogenesis in young animals and cell death in older ones. It suggests that neuronal cell death in such models is much more complex than believed...
- Effects of EGb 761 Ginkgo biloba extract on mitochondrial function and oxidative stressA Eckert
Department of Pharmacology, Biocenter, J W Goethe University of Frankfurt, Marie Curie Strasse 9, D 60439 Frankfurt am Main, Germany
Pharmacopsychiatry 36:S15-23. 2003..Our data further emphasize neuroprotective properties of EGb 761, such as protection against Abeta-toxicity, and antiapoptotic properties, which are probably due to its preventive effects on mitochondria...
- Impact of aging: sporadic, and genetic risk factors on vulnerability to apoptosis in Alzheimer's diseaseKatharina Schindowski
Department of Pharmacology, Biocenter, J W Goethe University of Frankfurt, Marie Curie Str 9, D 60439 Frankfurt am Main, Germany
Neuromolecular Med 4:161-78. 2003..In contrast, normal aging results in an increased susceptibility to apoptosis of both, CD4+ and CD8+ T cells...
- Early axonopathy preceding neurofibrillary tangles in mutant tau transgenic miceKarelle Leroy
Laboratory of Histology and Neuropathology, Universite Libre de Bruxelles, School of Medicine, 808, Route de Lennik, Bldg G, 1070 Brussels, Belgium
Am J Pathol 171:976-92. 2007..This Tg30tau model thus provides evidence that axonopathy precedes tangle formation and that both lesions can be dissociated from overt neuronal loss in selected brain areas but not from neuronal dysfunction...
- Age-related impairment of human T lymphocytes' activation: specific differences between CD4(+) and CD8(+) subsetsKatharina Schindowski
Department of Pharmacology, Johann Wolfgang Goethe University Biocenter, Marie Curie Strasse 9, 60439 Frankfurt Main, Germany
Mech Ageing Dev 123:375-90. 2002..The results will be discussed in relation to their relevance in neurodegenerative and psychiatric disorders...
- Enlarged infarct volume and loss of BDNF mRNA induction following brain ischemia in mice lacking FGF-2Irina Kiprianova
Interdisciplinary Center for Neurosciences, Department of Neuroanatomy, University of Heidelberg, D 69120 Heidelberg, Germany
Exp Neurol 189:252-60. 2004..Together, our data provide the first evidence that endogenous FGF-2 is important in coping with ischemic brain damage suggesting fgf2 as one crucial target gene for new therapeutic strategies in brain ischemia...
- p25/Cdk5-mediated retinoblastoma phosphorylation is an early event in neuronal cell deathMalika Hamdane
INSERM U422, Institut de Médecine Prédictive et Recherche Thérapeutique, Universite de Lille 2, Place de Verdun, 59045 Lille Cedex, France
J Cell Sci 118:1291-8. 2005..Hence, Rb might be an appropriate candidate that connects Cdk5 to cell-cycle deregulation during neuronal cell death...