High molecular weight amyloid β 1‐42 oligomers induce neurotoxicity via plasma membrane damage-Reference-Cited by-同舟云学术

High molecular weight amyloid β 1‐42 oligomers induce neurotoxicity via plasma membrane damage

Published:2019-05-13 Issue:8 Volume:33 Page:9220-9234
ISSN:0892-6638
Container-title:The FASEB Journal
language:en
Short-container-title:FASEB j.

Author:

Yasumoto Taro¹²,Takamura Yusaku³,Tsuji Mayumi²,Watanabe‐Nakayama Takahiro⁴,Imamura Keiko⁵⁶⁷,Inoue Haruhisa⁵⁶⁷,Nakamura Shiro⁸,Inoue Tomio⁸,Kimura Atsushi¹²,Yano Satoshi¹,Nishijo Hisao³,Kiuchi Yuji²,Teplow David B.⁹,Ono Kenjiro¹

Affiliation:

1. Division of Neurology Department of Internal Medicine Showa University Tokyo Japan

2. Department of Pharmacology School of Medicine Showa University Tokyo Japan

3. System Emotional Science Graduate School of Medicine and Pharmaceutical Sciences University of Toyama Toyama Japan

4. World Premier International Research Center Initiative (WPI) Nano Life Science Institute Kanazawa University Kakuma‐machi Kanazawa Japan

5. Center for iPS Cell Research and Application (CiRA) Kyoto University Kyoto Japan

6. iPSC‐based Drug Discovery and Development Team Riken BioResource Research Center (BRC) Kyoto Japan

7. Medical‐risk Avoidance based on iPS Cells Team Riken Center for Advanced Intelligence Project (AIP) Kyoto Japan

8. Department of Oral Physiology School of Dentistry Showa University Tokyo Japan

9. Department of Neurology David Geffen School of Medicine University of California‐Los Angeles (UCLA) Los Angeles California USA

Funder

Japan Society for the Promotion of Science

Japan Agency for Medical Research and Development

Publisher

Wiley

Subject

Genetics,Molecular Biology,Biochemistry,Biotechnology

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1096/fj.201900604R

Reference66 articles.

1. The amyloid hypothesis of Alzheimer's disease at 25 years

2. The Amyloid Hypothesis of Alzheimer's Disease: Progress and Problems on the Road to Therapeutics

3. Alzheimer's disease as oligomeropathy

4. Protofibrillar Intermediates of Amyloid β-Protein Induce Acute Electrophysiological Changes and Progressive Neurotoxicity in Cortical Neurons

5. Naturally secreted oligomers of amyloid β protein potently inhibit hippocampal long-term potentiation in vivo

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