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A beta(38) in the B...
A beta(38) in the Brains of Patients with Sporadic and Familial Alzheimer's Disease and Transgenic Mouse Models
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Reinert, Jochim (författare)
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Martens, Henrik (författare)
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Huettenrauch, Melanie (författare)
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Kolbow, Tekla (författare)
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- Lannfelt, Lars (författare)
- Uppsala universitet,Geriatrik
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- Ingelsson, Martin (författare)
- Uppsala universitet,Geriatrik
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Paetau, Anders (författare)
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Verkkoniemi-Ahola, Auli (författare)
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Bayer, Thomas A. (författare)
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Wirths, Oliver (författare)
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(creator_code:org_t)
- 2014
- 2014
- Engelska.
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Ingår i: Journal of Alzheimer's Disease. - 1387-2877 .- 1875-8908. ; 39:4, s. 871-881
- Relaterad länk:
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https://urn.kb.se/re...
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https://doi.org/10.3...
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Abstract
Ämnesord
Stäng
- The pathogenesis of Alzheimer's disease (AD) is believed to be closely dependent on deposits of neurotoxic amyloid-beta peptides (A beta), which become abundantly present throughout the central nervous system in advanced stages of the disease. The different A beta peptides existing are generated by subsequent cleavage of the amyloid-beta protein precursor (A beta PP) and may vary in length and differ at their C-terminus. Despite extensive studies on the most prevalent species A beta(40) and A beta(42), A beta peptides with other C-termini such as A beta(38) have not received much attention. In the present study, we used a highly specific and sensitive antibody against A beta(38) to analyze the distribution of this A beta species in cases of sporadic and familial AD, as well as in the brains of a series of established transgenic AD mouse models. We found A beta(38) to be present as vascular deposits in the brains of the majority of sporadic AD cases, whereas it is largely absent in non-demented control cases. A beta(38)-positive extracellular plaques were virtually limited to familial cases. Interestingly we observed A beta(38)-positive plaques not only among familial cases due to A beta PP mutations, but also in cases of familial AD caused by presenilin (PSEN) mutations. Furthermore we demonstrate that A beta(38) deposits in the form of extracellular plaques are common in several AD transgenic mouse models carrying either only A beta PP, or combinations of A beta PP, PSEN1, and tau transgenes.
Nyckelord
- A beta(38)
- A beta PP
- amyloid
- mutations
- presenilin
- transgenic mice
- vasculature
- vessels
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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