Research Topics
| Dietmar Rudolf ThalSummaryAffiliation: University of Ulm Country: Germany Publications
| Collaborators
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Detail Information
Publications
Vascular dementia: different forms of vessel disorders contribute to the development of dementia in the elderly brainDietmar Rudolf Thal
Institute of Pathology, Laboratory of Neuropathology, University of Ulm, Ulm, Germany
Exp Gerontol 47:816-24. 2012..As such, it seems to be important for clinical practice to consider treatment of potentially coexisting AD pathology in cognitively impaired patients with vascular lesions...
The role of astrocytes in amyloid β-protein toxicity and clearanceDietmar Rudolf Thal
Institute of Pathology, Laboratory of Neuropathology, Center for Biomedical Research, University of Ulm, Helmholtzstr 8 1, D 89081 Ulm, Germany
Exp Neurol 236:1-5. 2012....- Vascular pathology in the aged human brainLea Tenenholz Grinberg
Department of Neurology, University of California San Francisco, 305 Parnassus Avenue, San Francisco, CA 94143, USA
Acta Neuropathol 119:277-90. 2010.... - The pre-capillary segment of the blood-brain barrier and its relation to perivascular drainage in Alzheimer's disease and small vessel diseaseDietmar R Thal
Institute of Pathology Laboratory of Neuropathology, University of Ulm, Germany
ScientificWorldJournal 9:557-63. 2009.... - Stages of granulovacuolar degeneration: their relation to Alzheimer's disease and chronic stress responseDietmar Rudolf Thal
Laboratory of Neuropathology, Institute of Pathology, Center for Clinical Research, University of Ulm, Germany
Acta Neuropathol 122:577-89. 2011..Moreover, the association of the GVD stages with those of AD-related pathology but not with other neurodegenerative disorders points to a possible role of GVD and the response to chronic stress in the pathogenesis of AD... - Capillary cerebral amyloid angiopathy identifies a distinct APOE epsilon4-associated subtype of sporadic Alzheimer's diseaseDietmar Rudolf Thal
Institute of Pathology, University of Ulm, Albert Einstein Allee 11, Ulm, Germany
Acta Neuropathol 120:169-83. 2010.... - Parenchymal and vascular Abeta-deposition and its effects on the degeneration of neurons and cognition in Alzheimer's diseaseDietmar Rudolf Thal
Institute of Pathology Laboratory of Neuropathology University of Ulm, Ulm, Germany
J Cell Mol Med 12:1848-62. 2008..Therefore, it seems to be necessary to protect the brain from Abeta-toxicity already in stages of the disease with minor neuron loss before the onset of cognitive symptoms... - Cerebral amyloid angiopathy and its relationship to Alzheimer's diseaseDietmar Rudolf Thal
Laboratory of Neuropathology, Institute of Pathology, University of Ulm, Albert Einstein Allee 7, 89081 Ulm, Germany
Acta Neuropathol 115:599-609. 2008..Thus, blood flow alterations with subsequent hypoperfusion induced by CAA-related capillary occlusion presumably point to a second mechanism in which A beta adversely affects the brain in AD in addition to its direct neurotoxic effects... - Capillary cerebral amyloid angiopathy is associated with vessel occlusion and cerebral blood flow disturbancesDietmar Rudolf Thal
Department of Neuropathology, University of Bonn, D 53105 Bonn, Germany
Neurobiol Aging 30:1936-48. 2009..These results indicate that capillary CAA can result in capillary occlusion and is associated with cerebral blood flow disturbances providing an additional mechanism for toxic effects of the amyloid beta-protein in AD... - Tracing of temporo-entorhinal connections in the human brain: cognitively impaired argyrophilic grain disease cases show dendritic alterations but no axonal disconnection of temporo-entorhinal association neuronsDietmar Rudolf Thal
Department of Pathology, Laboratory of Neuropathology, University of Ulm, Ulm, Germany
Acta Neuropathol 115:175-83. 2008..Our findings in three cognitively impaired AGD cases suggest that AGD-related dementia constitutes a distinct disorder with a characteristic pattern of degeneration in the neuronal network... - Amyloid-β protein modulates the perivascular clearance of neuronal apolipoprotein E in mouse models of Alzheimer's diseaseHarshvardhan Rolyan
Laboratory of Neuropathology, Institute of Pathology, University of Ulm, Ulm, Germany
J Neural Transm 118:699-712. 2011..Thus, the production of Aβ and its interaction with apoE lead to the pathological perivascular drainage of neuronal apoE and provide insight into the pathological interactions of Aβ with neuronal apoE metabolism... 
Apolipoprotein E co-localizes with newly formed amyloid beta-protein (Abeta) deposits lacking immunoreactivity against N-terminal epitopes of Abeta in a genotype-dependent mannerDietmar Rudolf Thal
Department of Neuropathology, University of Bonn, Sigmund Freud Str 25, 53127 Bonn, Germany
Acta Neuropathol 110:459-71. 2005..Moreover, apoE-positive newly formed plaques were seen more frequently in APOE epsilon4/4 cases than in non-APOE epsilon4/4 individuals, thereby underlining the potentially crucial role of apoE for the development of Abeta deposits...- Selective vulnerability of different types of commissural neurons for amyloid beta-protein-induced neurodegeneration in APP23 mice correlates with dendritic tree morphologyEstibaliz Capetillo-Zarate
Department of Neuropathology, University of Bonn, Bonn, Germany
Brain 129:2992-3005. 2006..The vulnerability of different types of neurons to Abeta, thereby, is presumably related to the complexity of their dendritic morphology... - Transgenic expression of intraneuronal Aβ42 but not Aβ40 leads to cellular Aβ lesions, degeneration, and functional impairment without typical Alzheimer's disease pathologyDorothee Abramowski
Novartis Institutes for BioMedical Research, CH 4056 Basel, Switzerland
J Neurosci 32:1273-83. 2012..While intracellular membrane expression of Aβ1-42 in APP48 mice does not lead to the AD-typical lesions, Aβ aggregates develop within cells accompanied by considerable neurodegeneration... - Cerebral small vessel disease-induced apolipoprotein E leakage is associated with Alzheimer disease and the accumulation of amyloid beta-protein in perivascular astrocytesSabrina Utter
Department of Neuropathology, University of Bonn, Bonn, Germany
J Neuropathol Exp Neurol 67:842-56. 2008..It is therefore tempting to speculate that apoE represents a pathogenetic link between SVD and AD... - Dispersible amyloid β-protein oligomers, protofibrils, and fibrils represent diffusible but not soluble aggregates: their role in neurodegeneration in amyloid precursor protein (APP) transgenic miceAjeet Rijal Upadhaya
Laboratory of Neuropathology, Institute of Pathology, Center for Clinical Research at the University of Ulm, Ulm, Germany
Neurobiol Aging 33:2641-60. 2012..The concentration of dispersible Aβ aggregates, thereby, presumably determines its toxicity... - Occurrence and co-localization of amyloid beta-protein and apolipoprotein E in perivascular drainage channels of wild-type and APP-transgenic miceDietmar Rudolf Thal
Department of Neuropathology, University of Bonn Medical Center, Bonn, Germany
Neurobiol Aging 28:1221-30. 2007..In so doing, our results strengthen the hypothesis that an alteration of perivascular drainage supports Abeta-deposition and the development of AD... - Age-related appearance of dendritic inclusions in catecholaminergic brainstem neuronsHeiko Braak
Clinical Neuroanatomy, Center for Biomedical Research, Department of Neurology, University of Ulm, Ulm, Germany
Neurobiol Aging 34:286-97. 2013.... - High-molecular weight Aβ oligomers and protofibrils are the predominant Aβ species in the native soluble protein fraction of the AD brainAjeet Rijal Upadhaya
Laboratory of Neuropathology Institute of Pathology, Center for Clinical Research at the University of Ulm, Ulm, Germany
J Cell Mol Med 16:287-95. 2012..Thus, soluble hiMWAβ aggregates may play an important role in the pathogenesis of AD either independently or as a reservoir for release of loMWAβ oligomers... - Neurodegeneration in normal brain aging and diseaseDietmar Rudolf Thal
Department of Neuropathology, University of Bonn Medical Center, Sigmund Freud Strasse 25, D 53105 Bonn, Germany
Sci Aging Knowledge Environ 2004:pe26. 2004..Aging is, therefore, a major risk factor for these diseases but does not necessarily lead to age-related diseases... - Telomere shortening reduces Alzheimer's disease amyloid pathology in miceHarshvardhan Rolyan
Department of Molecular Medicine and Max Planck Research Department for Stem Cell Aging, University of Ulm, D 89081 Ulm, Germany
Brain 134:2044-56. 2011.... - Neuromyelitis optica lesions may inform multiple sclerosis heterogeneity debateWolfgang Bruck
Department of Neuropathology, University Medical Center, Georg August University, Gottingen, Germany
Ann Neurol 72:385-94. 2012..The aim of our study was to compare the histological characteristics of early active demyelinating NMO and MS brain lesions... - Telomere shortening impairs regeneration of the olfactory epithelium in response to injury but not under homeostatic conditionsMasami Watabe-Rudolph
Department of Otorhinolaryngology, University of Ulm, Ulm, Germany
PLoS ONE 6:e27801. 2011..These findings could be relevant for the impairment in OE function in elderly people... - Expression of alpha2-macroglobulin, neutrophil elastase, and interleukin-1alpha differs in early-stage and late-stage atherosclerotic lesions in the arteries of the circle of WillisSergey Larionov
Department of Neuropathology, University of Bonn, Sigmund Freud Strasse 25, 53105, Bonn, Germany
Acta Neuropathol 113:33-43. 2007..Therefore, our findings support the hypothesis that NE-induced tissue damage in late-stage AS plaques contributes to the development of plaque rupture and subsequent thrombosis... - Vascular pathology in Alzheimer disease: correlation of cerebral amyloid angiopathy and arteriosclerosis/lipohyalinosis with cognitive declineDietmar Rudolf Thal
Department of Neuropathology, University of Bonn Medical Center, Bonn, Germany
J Neuropathol Exp Neurol 62:1287-301. 2003..A combination of both CAA and AS/LH may, therefore, contribute to neurodegeneration in AD. These data also suggest that small vessel disease due to arteriosclerosis and fibrolipohyalinosis is a potential target for the treatment of AD... - Homozygosity for the K variant of BCHE gene increases the risk for development of neurofibrillary pathology but not amyloid deposits at young agesEstifanos Ghebremedhin
Institute of Clinical Neuroanatomy, J W Goethe University, Theodor Stern Kai 7, 60590 Frankfurt Main, Germany
Acta Neuropathol 114:359-63. 2007..These findings suggest that homozygosity, but not heterozygosity, for BCHE-K is a potential risk factor for the development of NFT pathology in young individuals implicating BCHE-K in the pathogenesis of early AD... - Two types of sporadic cerebral amyloid angiopathyDietmar Rudolf Thal
Department of Clinical Neuroanatomy, J.W. Goethe University, Frankfurt am Main, Germany
J Neuropathol Exp Neurol 61:282-93. 2002..CAA-Type 2 is not associated with the epsilon4 allele as a risk factor but shows a higher epsilon2 allele frequency than CAA-Type 1 cases and controls in our sample...