N-truncated Aβ4–x peptides in sporadic Alzheimer’s disease cases and transgenic Alzheimer mouse models
Author:
Funder
Alzheimer Forschung Initiative
Stiftung VERUM
Publisher
Springer Science and Business Media LLC
Subject
Cognitive Neuroscience,Neurology (clinical),Neurology
Link
http://link.springer.com/content/pdf/10.1186/s13195-017-0309-z.pdf
Reference40 articles.
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3. O’Brien RJ, Wong PC. Amyloid precursor protein processing and Alzheimer’s disease. Annu Rev Neurosci. 2011;34:185–204.
4. Beher D, Wrigley JD, Owens AP, Shearman MS. Generation of C-terminally truncated amyloid-β peptides is dependent on γ-secretase activity. J Neurochem. 2002;82:563–75.
5. Reinert J, Richard BC, Klafki HW, Friedrich B, Bayer TA, Wiltfang J, Kovacs GG, Ingelsson M, Lannfelt L, Paetau A, et al. Deposition of C-terminally truncated Aβ species Aβ37 and Aβ39 in Alzheimer’s disease and transgenic mouse models. Acta Neuropathol Commun. 2016;4:24.
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