Generation and deposition of Aβ43 by the virtually inactive presenilin‐1 L435F mutant contradicts the presenilin loss‐of‐function hypothesis of Alzheimer's disease-Reference-Cited by-同舟云学术

Generation and deposition of Aβ43 by the virtually inactive presenilin‐1 L435F mutant contradicts the presenilin loss‐of‐function hypothesis of Alzheimer's disease

Published:2016-03-17 Issue:5 Volume:8 Page:458-465
ISSN:1757-4676
Container-title:EMBO Molecular Medicine
language:en
Short-container-title:EMBO Mol Med

Author:

Kretner Benedikt¹²,Trambauer Johannes¹,Fukumori Akio²,Mielke Janina³,Kuhn Peer‐Hendrik²⁴,Kremmer Elisabeth⁵⁶,Giese Armin³,Lichtenthaler Stefan F²⁴⁵,Haass Christian¹²⁵,Arzberger Thomas²³⁷,Steiner Harald¹²

Affiliation:

1. Biomedical Center Metabolic Biochemistry Ludwig‐Maximilians‐University Munich Munich Germany

2. DZNE ‐ German Center for Neurodegenerative Diseases Munich Germany

3. Center for Neuropathology and Prion Research Ludwig‐Maximilians‐University Munich Munich Germany

4. Neuroproteomics, Klinikum rechts der Isar and Institute for Advanced Study Technische Universität München Munich Germany

5. Munich Cluster for Systems Neurology (SyNergy) Munich Germany

6. Institute of Molecular Immunology Helmholtz Zentrum München Munich Germany

7. Department of Psychiatry and Psychotherapy Ludwig‐Maximilians‐University Munich Munich Germany

Funder

Deutsche Forschungsgemeinschaft

European Research Council

Seventh Framework Programme

Publisher

EMBO

Subject

Molecular Medicine

Link

https://onlinelibrary.wiley.com/doi/pdf/10.15252/emmm.201505952

Reference37 articles.

1. Aβ43 is neurotoxic and primes aggregation of Aβ40 in vivo

2. Cellular Expression and Proteolytic Processing of Presenilin Proteins Is Developmentally Regulated During Neuronal Differentiation

3. The mechanism of γ-Secretase dysfunction in familial Alzheimer disease

4. Mutation of the β-amyloid precursor protein in familial Alzheimer's disease increases β-protein production

5. Reconstitution of γ-secretase activity

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