C-terminally truncated Amyloid-β peptides in Alzheimer’s dementia: Deposition of Aβ37, Aβ38, and Aβ39 in the brains of patients with sporadic and familiar Alzheimer’s dementia and in transgenic mouse models.

Reinert, Jochim

dc.contributor.advisor	Wirths, Oliver Prof. Dr.
dc.contributor.author	Reinert, Jochim
dc.date.accessioned	2018-01-24T10:07:58Z
dc.date.available	2018-02-01T23:50:43Z
dc.date.issued	2018-01-24
dc.identifier.uri	http://hdl.handle.net/11858/00-1735-0000-002E-E331-E
dc.identifier.uri	http://dx.doi.org/10.53846/goediss-6699
dc.identifier.uri	http://dx.doi.org/10.53846/goediss-6699
dc.language.iso	eng	de
dc.rights.uri	http://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subject.ddc	610	de
dc.title	C-terminally truncated Amyloid-β peptides in Alzheimer’s dementia: Deposition of Aβ37, Aβ38, and Aβ39 in the brains of patients with sporadic and familiar Alzheimer’s dementia and in transgenic mouse models.	de
dc.type	doctoralThesis	de
dc.contributor.referee	Wirths, Oliver Prof. Dr.
dc.date.examination	2018-01-25
dc.description.abstracteng	Alzheimer's dementia is a devastating neurodegenerative disease characterized by profound neuropathological changes of the brain. Imbalances in the production of aggregation-prone Amyloid-Beta Peptides are believed to play a pivotal role in disease pathogenesis. These peptides are generated by subsequent proteolysis of the Amyloid Precursor Protein by a Beta and a Gamma-Sekretase. This Proteolysis yields peptides of differing length with varying C-termini. While the presumably most toxic species Abeta42 and the most produced species Abeta40 have been subject to intensive research, C-terminally truncated Peptides have not received much attention. This study investigates the contribution of Abeta37, Abeta38, and Abeta39 to the neuropathological changes in sporadic and familial Alzheimer's dementia. C-terminally truncated Abeta peptides were found to be deposited primarily to the vasculature in sporadic cases, while familial cases presented more intense depositions that included neuritic plaques. Moreover, this study analyzed commonly employed transgenic mouse models for depositions of the C-terminally truncated Abeta peptides.	de
dc.contributor.coReferee	Stadelmann-Nessler, Christine Prof. Dr.
dc.subject.eng	Alzheimer's dementia	de
dc.subject.eng	Cerebral amyloid angiopathy	de
dc.subject.eng	Abeta38	de
dc.subject.eng	Abeta37	de
dc.subject.eng	Abeta39	de
dc.identifier.urn	urn:nbn:de:gbv:7-11858/00-1735-0000-002E-E331-E-7
dc.affiliation.institute	Medizinische Fakultät	de
dc.subject.gokfull	Medizin (PPN619874732)	de
dc.description.embargoed	2018-02-01
dc.identifier.ppn	101155173X

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Human- und Zahnmedizin [2873]

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