A5003366066- Alzheimer's disease research and treatments
- Neuroscience and Neuropharmacology Research
- Cholinesterase and Neurodegenerative Diseases
- Neurogenesis and neuroplasticity mechanisms
- Cancer-related Molecular Pathways
- Proteoglycans and glycosaminoglycans research
- Mitochondrial Function and Pathology
- Neuroinflammation and Neurodegeneration Mechanisms
- Nerve injury and regeneration
- Memory and Neural Mechanisms
- Dementia and Cognitive Impairment Research
- Pancreatitis Pathology and Treatment
- Advanced Glycation End Products research
- Microtubule and mitosis dynamics
- Parkinson's Disease Mechanisms and Treatments
- Pediatric Hepatobiliary Diseases and Treatments
- Neurological Disorders and Treatments
- RNA modifications and cancer
- Prion Diseases and Protein Misfolding
- Neuropeptides and Animal Physiology
- S100 Proteins and Annexins
- Nicotinic Acetylcholine Receptors Study
- Connective tissue disorders research
- Nuclear Receptors and Signaling
- Biochemical effects in animals
Leipzig University
2014-2024
TU Dresden
2023
The University of Texas Health Science Center at Tyler
2020
The University of Texas at Tyler
2020
Allen Institute for Brain Science
1999-2019
Paul Drude Institute for Solid State Electronics
1996-2019
Klinik und Poliklinik für Neurologie
2019
University Hospital Leipzig
1994-2019
University of Cologne
2008
Fischer (Germany)
2008
Alzheimer's disease (AD) is a degenerative disorder where the distribution of pathology throughout brain not random but follows predictive pattern used for pathological staging. While involvement defined functional systems fairly well established more advanced stages, initial sites degeneration are still ill defined. The prevailing concept suggests an origin within transentorhinal and entorhinal cortex (EC) from spreads to other areas. Still, this has been challenged recently suggesting...
Brain iron is an essential as well a toxic redox active element. Physiological levels are not uniform among the different cell types. Besides availability of quantitative methods, knowledge about brain lags behind. Thereby, disclosing mechanisms homeostasis helps to understand pathological iron-accumulations in diseased and aged brains. With our study we want contribute closing gap by providing data on concentration distribution neurons glial cells situ. Using nuclear microprobe scanning...
Neurofibrillary pathology [paired helical filaments (PHFs)] formed by the microtubule-associated protein tau in a hyperphosphorylated form is major hallmark of Alzheimer9s disease and related disorders. The process phosphorylation, thought to be critical importance for PHF formation, its potential link neurodegeneration, however, not understood very well, mostly because lack physiological <i>in vivo</i> model PHF-like phosphorylation. Here we describe formation highly phosphorylated tau,...
A relationship between the apolipoprotein E (apoE) genotype and risk to develop Alzheimer's disease has been established recently. Apolipoprotein synthesis is implicated in developmental processes neuronal repair of adult nervous system. In present study, we investigated influence polymorphism on severity degeneration extent plastic dendritic remodeling disease. Changes length arborization dendrites Golgi-impregnated neurons basal nucleus Meynert, locus coeruleus, raphe magnus nucleus,...
We have analyzed gene expression in various brain regions of humans and chimpanzees. Within both human chimpanzee individuals, the transcriptomes cerebral cortex are very similar to each other differ more between individuals than among within an individual. In contrast, cortex, caudate nucleus, cerebellum substantially from other. Between chimpanzees, 10% genes their at least one region brain. The majority these differences shared all regions. Whereas encoding proteins involved signal...
Reactivation of the cell cycle, including DNA replication, might play a major role in Alzheimer9s disease (AD). A more than diploid content differentiated neurons alternatively result from chromosome mis-segregation during mitosis neuronal progenitor cells. It was our objective to distinguish between these two mechanisms for aneuploidy and provide evidence functional cycle AD. Using slide-based cytometry, chromogenic <i>in situ</i> hybridization, PCR amplification <i>alu</i>-repeats, we...
RECENT evidence indicates that an impairment of neuronal adaptive and reparative processes might be a key feature the pathomechanism Alzheimer's disease. Aberrations in response are likely to result from alterations intracellular signal transduction cascades. As consequence abnormal signalling, activation those molecular events triggered neurones which, dividing cells, would lead cellular transformation. In present study, changes expression cyclin-dependent kinase inhibitor p16, regulator...
The microtubule-associated protein Tau is mainly expressed in neurons, where it binds and stabilizes microtubules. In Alzheimer disease other tauopathies, has a reduced affinity toward As consequence, detaches from microtubules eventually aggregates into β-sheet-containing filaments. fibrillization of monomeric to filaments multistep process that involves the formation various aggregates, including spherical protofibrillar oligomers. Previous concepts, primarily developed for Aβ α-synuclein,...