Dietmar Rudolf Thal

Summary

Affiliation: University of Ulm
Country: Germany

Publications

  1. doi The role of astrocytes in amyloid β-protein toxicity and clearance
    Dietmar 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
  2. pmc Vascular dementia: different forms of vessel disorders contribute to the development of dementia in the elderly brain
    Dietmar Rudolf Thal
    Institute of Pathology, Laboratory of Neuropathology, University of Ulm, Ulm, Germany
    Exp Gerontol 47:816-24. 2012
  3. pmc Vascular pathology in the aged human brain
    Lea Tenenholz Grinberg
    Department of Neurology, University of California San Francisco, 305 Parnassus Avenue, San Francisco, CA 94143, USA
    Acta Neuropathol 119:277-90. 2010
  4. doi Capillary cerebral amyloid angiopathy identifies a distinct APOE epsilon4-associated subtype of sporadic Alzheimer's disease
    Dietmar Rudolf Thal
    Institute of Pathology, University of Ulm, Albert Einstein Allee 11, Ulm, Germany
    Acta Neuropathol 120:169-83. 2010
  5. doi The pre-capillary segment of the blood-brain barrier and its relation to perivascular drainage in Alzheimer's disease and small vessel disease
    Dietmar R Thal
    Institute of Pathology Laboratory of Neuropathology, University of Ulm, Germany
    ScientificWorldJournal 9:557-63. 2009
  6. doi Parenchymal and vascular Abeta-deposition and its effects on the degeneration of neurons and cognition in Alzheimer's disease
    Dietmar Rudolf Thal
    Institute of Pathology Laboratory of Neuropathology University of Ulm, Ulm, Germany
    J Cell Mol Med 12:1848-62. 2008
  7. doi Cerebral amyloid angiopathy and its relationship to Alzheimer's disease
    Dietmar Rudolf Thal
    Laboratory of Neuropathology, Institute of Pathology, University of Ulm, Albert Einstein Allee 7, 89081 Ulm, Germany
    Acta Neuropathol 115:599-609. 2008
  8. doi Capillary cerebral amyloid angiopathy is associated with vessel occlusion and cerebral blood flow disturbances
    Dietmar Rudolf Thal
    Department of Neuropathology, University of Bonn, D 53105 Bonn, Germany
    Neurobiol Aging 30:1936-48. 2009
  9. pmc 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 neurons
    Dietmar Rudolf Thal
    Department of Pathology, Laboratory of Neuropathology, University of Ulm, Ulm, Germany
    Acta Neuropathol 115:175-83. 2008
  10. doi Stages of granulovacuolar degeneration: their relation to Alzheimer's disease and chronic stress response
    Dietmar Rudolf Thal
    Laboratory of Neuropathology, Institute of Pathology, Center for Clinical Research, University of Ulm, Germany
    Acta Neuropathol 122:577-89. 2011

Collaborators

Detail Information

Publications28

  1. doi The role of astrocytes in amyloid β-protein toxicity and clearance
    Dietmar 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
    ....
  2. pmc Vascular dementia: different forms of vessel disorders contribute to the development of dementia in the elderly brain
    Dietmar 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...
  3. pmc Vascular pathology in the aged human brain
    Lea Tenenholz Grinberg
    Department of Neurology, University of California San Francisco, 305 Parnassus Avenue, San Francisco, CA 94143, USA
    Acta Neuropathol 119:277-90. 2010
    ....
  4. doi Capillary cerebral amyloid angiopathy identifies a distinct APOE epsilon4-associated subtype of sporadic Alzheimer's disease
    Dietmar Rudolf Thal
    Institute of Pathology, University of Ulm, Albert Einstein Allee 11, Ulm, Germany
    Acta Neuropathol 120:169-83. 2010
    ....
  5. doi The pre-capillary segment of the blood-brain barrier and its relation to perivascular drainage in Alzheimer's disease and small vessel disease
    Dietmar R Thal
    Institute of Pathology Laboratory of Neuropathology, University of Ulm, Germany
    ScientificWorldJournal 9:557-63. 2009
    ....
  6. doi Parenchymal and vascular Abeta-deposition and its effects on the degeneration of neurons and cognition in Alzheimer's disease
    Dietmar 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...
  7. doi Cerebral amyloid angiopathy and its relationship to Alzheimer's disease
    Dietmar 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...
  8. doi Capillary cerebral amyloid angiopathy is associated with vessel occlusion and cerebral blood flow disturbances
    Dietmar 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...
  9. pmc 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 neurons
    Dietmar 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...
  10. doi Stages of granulovacuolar degeneration: their relation to Alzheimer's disease and chronic stress response
    Dietmar 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...
  11. doi Amyloid-β protein modulates the perivascular clearance of neuronal apolipoprotein E in mouse models of Alzheimer's disease
    Harshvardhan 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...
  12. ncbi Selective vulnerability of different types of commissural neurons for amyloid beta-protein-induced neurodegeneration in APP23 mice correlates with dendritic tree morphology
    Estibaliz 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...
  13. ncbi Apolipoprotein E co-localizes with newly formed amyloid beta-protein (Abeta) deposits lacking immunoreactivity against N-terminal epitopes of Abeta in a genotype-dependent manner
    Dietmar 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...
  14. doi Transgenic expression of intraneuronal Aβ42 but not Aβ40 leads to cellular Aβ lesions, degeneration, and functional impairment without typical Alzheimer's disease pathology
    Dorothee 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...
  15. ncbi Occurrence and co-localization of amyloid beta-protein and apolipoprotein E in perivascular drainage channels of wild-type and APP-transgenic mice
    Dietmar 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...
  16. doi Cerebral small vessel disease-induced apolipoprotein E leakage is associated with Alzheimer disease and the accumulation of amyloid beta-protein in perivascular astrocytes
    Sabrina 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...
  17. doi Dispersible amyloid β-protein oligomers, protofibrils, and fibrils represent diffusible but not soluble aggregates: their role in neurodegeneration in amyloid precursor protein (APP) transgenic mice
    Ajeet 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...
  18. doi Age-related appearance of dendritic inclusions in catecholaminergic brainstem neurons
    Heiko Braak
    Clinical Neuroanatomy, Center for Biomedical Research, Department of Neurology, University of Ulm, Ulm, Germany
    Neurobiol Aging 34:286-97. 2013
    ....
  19. doi Biochemical stages of amyloid-β peptide aggregation and accumulation in the human brain and their association with symptomatic and pathologically preclinical Alzheimer's disease
    Ajeet Rijal Upadhaya
    1 Laboratory of Neuropathology, Institute of Pathology, Centre for Clinical Research at the University of Ulm, Ulm, Germany
    Brain 137:887-903. 2014
    ....
  20. doi High-molecular weight Aβ oligomers and protofibrils are the predominant Aβ species in the native soluble protein fraction of the AD brain
    Ajeet 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...
  21. ncbi Neurodegeneration in normal brain aging and disease
    Dietmar 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...
  22. doi Telomere shortening reduces Alzheimer's disease amyloid pathology in mice
    Harshvardhan 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
    ....
  23. doi Neuromyelitis optica lesions may inform multiple sclerosis heterogeneity debate
    Wolfgang 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...
  24. pmc Telomere shortening impairs regeneration of the olfactory epithelium in response to injury but not under homeostatic conditions
    Masami 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...
  25. ncbi 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 Willis
    Sergey 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...
  26. ncbi Vascular pathology in Alzheimer disease: correlation of cerebral amyloid angiopathy and arteriosclerosis/lipohyalinosis with cognitive decline
    Dietmar 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...
  27. ncbi Homozygosity for the K variant of BCHE gene increases the risk for development of neurofibrillary pathology but not amyloid deposits at young ages
    Estifanos 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...
  28. ncbi Two types of sporadic cerebral amyloid angiopathy
    Dietmar 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...