β-amyloid redirects norepinephrine signaling to activate the pathogenic GSK3β/tau cascade

Author:

Zhang Fang1ORCID,Gannon Mary1ORCID,Chen Yunjia1,Yan Shun2ORCID,Zhang Sixue3ORCID,Feng Wendy1ORCID,Tao Jiahui1ORCID,Sha Bingdong1ORCID,Liu Zhenghui4,Saito Takashi5ORCID,Saido Takaomi5ORCID,Keene C. Dirk6ORCID,Jiao Kai2ORCID,Roberson Erik D.7ORCID,Xu Huaxi8,Wang Qin1ORCID

Affiliation:

1. Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.

2. Department of Genetics, University of Alabama at Birmingham, Birmingham, AL 35294, USA.

3. Department of Chemistry, Southern Research Institute, Birmingham, AL 35205, USA.

4. Department of Microbiology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.

5. Laboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama 351-0198, Japan.

6. Department of Pathology, University of Washington, Seattle, WA 98104, USA.

7. Alzheimer’s Disease Center, Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.

8. Neuroscience Initiative, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037, USA.

Abstract

Noradrenergic signaling sensitizes pathological GSK3β/tau activation to nanomolar Aβ.

Funder

National Institute of Mental Health

National Institute on Aging

National Institute of Neurological Disorders and Stroke

Publisher

American Association for the Advancement of Science (AAAS)

Subject

General Medicine

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