Zobrazeno 1 - 10
of 28
pro vyhledávání: '"Henrike Hartmann"'
Autor:
Henrike Hartmann, Hans Clevers, Viet Minh Do, Bernd Sommer, Matthias Staufenbiel, Christine Sturchler-Pierrat, Paul Saftig, Zhuohua Zhang, Xi He, M. Van De Wetering, B. De Strooper, Dorothee Abramowski, Bruce A. Yankner
Publikováno v:
Nature. 395:698-702
Mutations of the presenilin-1 gene are a major cause of familial early-onset Alzheimer's disease. Presenilin-1 can associate with members of the catenin family of signalling proteins, but the significance of this association is unknown. Here we show
Autor:
Jorge Busciglio, Henrike Hartmann, Matthias Staufenbiel, Bruce A. Yankner, Karl-Heinz Baumann
Publikováno v:
Journal of Biological Chemistry. 272:14505-14508
Most cases of early-onset familial Alzheimer's disease are caused by mutations in the presenilin genes. Presenilin-1 (PS1) is subject to proteolytic cleavage resulting in the accumulation of N- and C-terminal fragments. In this report, we show that t
Publikováno v:
Life Sciences. 59:435-449
Age-related changes in resting levels of the free intracellular calcium concentration ([Ca2+]i) as well as alterations of the rise in [Ca2+]i following depolarization have been investigated in acutely isolated cells of the mouse brain and of various
Publikováno v:
Amyloid. 3:234-241
The β-amyloid peptide (Aβ) has been shown to possess neurotoxic properties, suggesting that the peptide may be involved in neurodegenerative processes occurring during AD. On the other hand, low concentrations of Aβ have been shown to be neurotrop
Publikováno v:
Biochemical and Biophysical Research Communications. 200:1185-1192
Besides the neurotoxic properties of beta-amyloid (beta A4), apolipoprotein E polymorphism seems to play an important role in the pathogenesis of sporadic Alzheimer's disease (AD). The calcium amplifying effect of beta A25-35 (the neurotoxic sequence
Publikováno v:
European Archives of Psychiatry and Clinical Neuroscience. 243:218-223
Several studies suggest that alterations of cytosolic free calcium concentration ([Ca2+]i) are involved in the pathophysiology of aging and Alzheimer's disease (AD). However, only few data are presently available giving detailed information about spe
Publikováno v:
Life Sciences. 55:2019-2029
Because of its function as an intracellular messenger in many cells, calcium plays an important role in signal transduction. Changes in intracellular free calcium concentration occur in central neurons during aging and Alzheimer's disease (AD). It is
Publikováno v:
Life Sciences. 55:2011-2018
Maintenance of the cellular calcium homeostasis plays an important role for neuronal cell function and interneuronal cell to cell communication. Therefore, alterations of the neuronal Ca2+ homeostasis may play a crucial role for brain aging in genera
Publikováno v:
FEBS Letters. 330:49-52
The role of beta-amyloid in Alzheimer's disease and its cellular mechanism of action on neurons are still unclear. There is growing evidence that beta-amyloid or its fragment, 25-35, influence neuronal calcium regulation. To investigate the effects o
Autor:
Henrike Hartmann, Bruce A. Yankner
The majority of familial Alzheimer's disease (AD) cases are linked to mutations of the presenilin 1 and 2 (PS1, PS2) genes on chromosomes 14 and 1, respectively (1-3). PS1 and PS2 are about 67% identical in amino acid sequence. Based on hydrophobicit
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::7cfb989290e794961c2acb163ab00f2c
https://doi.org/10.1385/1-59259-195-7:297
https://doi.org/10.1385/1-59259-195-7:297