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Deposition of C-ter...
Deposition of C-terminally truncated A beta species A beta 37 and A beta 39 in Alzheimer's disease and transgenic mouse models
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Reinert, Jochim (författare)
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Richard, Bernhard C. (författare)
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Klafki, Hans W. (författare)
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Friedrich, Beate (författare)
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Bayer, Thomas A. (författare)
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Wiltfang, Jens (författare)
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Kovacs, Gabor G. (författare)
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Ingelsson, Martin, 1965- (författare)
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Lannfelt, Lars (författare)
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Paetau, Anders (författare)
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Bergquist, Jonas (författare)
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Wirths, Oliver (författare)
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- 2016
- 2016
- Engelska.
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Ingår i: Acta neuropathologica communications. - 1509-409X. ; 4
Abstract
Ämnesord
Stäng
- In Alzheimer's disease (AD) a variety of amyloid beta-peptides (A beta) are deposited in the form of extracellular diffuse and neuritic plaques (NP), as well as within the vasculature. The generation of A beta from its precursor, the amyloid precursor protein (APP), is a highly complex procedure that involves subsequent proteolysis of APP by beta-and gamma-secretases. Brain accumulation of A beta due to impaired A beta degradation and/or altered ratios between the different A beta species produced is believed to play a pivotal role in AD pathogenesis. While the presence of A beta 40 and A beta 42 in vascular and parenchymal amyloid have been subject of extensive studies, the deposition of carboxyterminal truncated A beta peptides in AD has not received comparable attention. In the current study, we for the first time demonstrate the immunohistochemical localization of A beta 37 and A beta 39 in human sporadic AD (SAD). Our study further included the analysis of familial AD (FAD) cases carrying the APP mutations KM670/671NL, E693G and I716F, as well as a case of the PSEN1 Delta Exon9 mutation. A beta 37 and A beta 39 were found to be widely distributed within the vasculature in the brains of the majority of studied SAD and FAD cases, the latter also presenting considerable amounts of A beta 37 containing NPs. In addition, both peptides were found to be present in extracellular plaques but only scarce within the vasculature in brains of a variety of transgenic AD mouse models. Taken together, our study indicates the importance of C-terminally truncated A beta in sporadic and familial AD and raises questions about how these species are generated and regulated.
Ämnesord
- Medical and Health Sciences (hsv)
- Clinical Medicine (hsv)
- Neurology (hsv)
- Medicin och hälsovetenskap (hsv)
- Klinisk medicin (hsv)
- Neurologi (hsv)
Nyckelord
- Alzheimer
- C-terminal truncation
- Amyloid precursor protein
- Transgenic mice
- A beta 37
- A beta 39
- Immunohistochemistry
- Mass spectrometry
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Till lärosätets databas
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Reinert, Jochim
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Richard, Bernhar ...
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Klafki, Hans W.
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Friedrich, Beate
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Bayer, Thomas A.
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Wiltfang, Jens
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visa fler...
-
Kovacs, Gabor G.
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Ingelsson, Marti ...
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Lannfelt, Lars
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Paetau, Anders
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Bergquist, Jonas
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Wirths, Oliver
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visa färre...
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