Thal, Dietmar Rudolf

Capillary CAA and perivascular Aβ-deposition: Two distinct features of Alzheimer's disease pathology

Attems, J., Yamaguchi, H., Saido, T. C., & Thal, D. R. (2010) · Journal of the Neurological Sciences

Alzheimer's disease research and treatmentsIntracerebral and Subarachnoid Hemorrhage Research

Cited by 63

Progression of neurofibrillary changes and PHF-τ in end-stage Alzheimer’s disease is different from plaque and cortical microglial pathology

Thal, D. R., Arendt, T., Waldmann, G., Holzer, M., Zedlick, D., Rüb, U., & Schober, R. (1998) · Neurobiology of Aging

Alzheimer's disease research and treatmentsDementia and Cognitive Impairment Research

Cited by 53

Apolipoprotein E co-localizes with newly formed amyloid β-protein (Aβ) deposits lacking immunoreactivity against N-terminal epitopes of Aβ in a genotype-dependent manner

Thal, D. R., Capetillo-Zarate, E., Schultz, C., Rüb, U., Saido, T. C., Yamaguchi, H., Haass, C., Griffin, W. S. T., Del Tredici, K., Braak, H., et al. (2005) · Acta Neuropathologica

Alzheimer's disease research and treatmentsDementia and Cognitive Impairment Research

Cited by 50

Selective vulnerability of different types of commissural neurons for amyloid -protein-induced neurodegeneration in APP23 mice correlates with dendritic tree morphology

Capetillo-Zarate, E., Staufenbiel, M., Abramowski, D., Haass, C., Escher, A., Stadelmann, C., Yamaguchi, H., Wiestler, O. D., & Thal, D. R. (2006) · Brain

Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration Mechanisms

Cited by 45

Oligodendroglia in cortical multiple sclerosis lesions decrease with disease progression, but regenerate after repeated experimental demyelination

Rodriguez, E. G., Wegner, C., Kreutzfeldt, M., Neid, K., Thal, D. R., Jürgens, T., Brück, W., Stadelmann, C., & Merkler, D. (2014) · Acta Neuropathologica

Multiple Sclerosis Research StudiesNeurogenesis and neuroplasticity mechanisms

Cited by 44

Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology

Suelves, N., Saleki, S., Ibrahim, T., Palomares, D., Moonen, S., Koper, M. J., Vrancx, C., Vadukul, D. M., Papadopoulos, N., Viceconte, N., et al. (2023) · Acta Neuropathologica Communications

Alzheimer's disease research and treatmentsAutophagy in Disease and Therapy

Cited by 43

Transgenic Expression of Intraneuronal Aβ 42 But Not Aβ 40 Leads to Cellular Aβ Lesions, Degeneration, and Functional Impairment without Typical Alzheimer's Disease Pathology

Abramowski, D., Rabe, S., Upadhaya, A. R., Reichwald, J., Danner, S., Staab, D., Capetillo-Zarate, E., Yamaguchi, H., Saido, T. C., Wiederhold, K.-H., et al. (2012) · The Journal of Neuroscience

Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration Mechanisms

Cited by 41

CYSTEINE-SPARING NOTCH3 MUTATIONS: CADASIL OR CADASIL VARIANTS?

Scheid, R., Heinritz, W., Leyhe, T., Thal, D. R., Schober, R., Strenge, S., von Cramon, D. Y., & Froster, U. G. (2008) · Neurology

Cerebrovascular and genetic disordersGenetic Neurodegenerative Diseases

Cited by 31

Mapping the sequence specificity of heterotypic amyloid interactions enables the identification of aggregation modifiers

Louros, N., Ramakers, M., Michiels, E., Konstantoulea, K., Morelli, C., Garcia, T., Moonen, N., D’Haeyer, S., Goossens, V., Thal, D. R., et al. (2022) · Nature Communications

Alzheimer's disease research and treatmentsPrion Diseases and Protein Misfolding

Cited by 28

Sequence of proteome profiles in preclinical and symptomatic Alzheimer's disease

Li, X., Tsolis, K. C., Koper, M. J., Ronisz, A., Ospitalieri, S., von Arnim, C. A. F., Vandenberghe, R., Tousseyn, T., Scheuerle, A., Economou, A., et al. (2021) · Alzheimer's & Dementia

Alzheimer's disease research and treatmentsDementia and Cognitive Impairment Research

Cited by 27