Aβ-accelerated neurodegeneration caused by Alzheimer’s-associated ACE variant R1279Q is rescued by angiotensin system inhibition in mice

Author:

Cuddy Leah K.1ORCID,Prokopenko Dmitry2ORCID,Cunningham Eric P.1ORCID,Brimberry Ross1,Song Peter1ORCID,Kirchner Rory3ORCID,Chapman Brad A.3,Hofmann Oliver4ORCID,Hide Winston5ORCID,Procissi Daniele6ORCID,Hanania Taleen7ORCID,Leiser Steven C.7,Tanzi Rudolph E2ORCID,Vassar Robert18ORCID

Affiliation:

1. Ken and Ruth Davee Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.

2. Genetics and Aging Unit and McCance Center for Brain Health, Department of Neurology, Massachusetts General Hospital, Boston, MA 02129, USA.

3. Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.

4. Department of Clinical Pathology, University of Melbourne, Victoria 3000, Melbourne, Australia.

5. Department of Pathology, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA.

6. Department of Radiology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.

7. PsychoGenics Inc., Paramus, NJ 07652, USA.

8. Mesulam Center for Cognitive Neurology and Alzheimer’s Disease, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.

Abstract

Ace1 knockin mice have increased neuronal ACE1 and hippocampal neuron loss that is accelerated by Aβ and blocked by approved angiotensin pathway drugs.

Funder

National Institutes of Health

JPB Foundation

Cure Alzheimer’s Fund

Publisher

American Association for the Advancement of Science (AAAS)

Subject

General Medicine

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