Endosomal recycling reconciles the Alzheimer’s disease paradox-Reference-Cited by-同舟云学术

Endosomal recycling reconciles the Alzheimer’s disease paradox

Published:2020-12-02 Issue:572 Volume:12 Page:
ISSN:1946-6234
Container-title:Science Translational Medicine
language:en
Short-container-title:Sci. Transl. Med.

Author:

Small Scott A.¹^ORCID,Petsko Gregory A.²^ORCID

Affiliation:

1. Alzheimer’s Disease Research Center, Department of Neurology, Columbia University, New York, NY 10032, USA.

2. Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02115, USA.

Abstract

A hub-and-spoke model with endosomal recycling as the hub can reconcile the pathogenic contribution of amyloid precursor protein to Alzheimer’s disease.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

General Medicine

Reference9 articles.

1. Persistent neuropathological effects 14 years following amyloid-β immunization in Alzheimer’s disease

2. Depletion of the AD Risk Gene SORL1 Selectively Impairs Neuronal Endosomal Traffic Independent of Amyloidogenic APP Processing

3. A Large Panel of Isogenic APP and PSEN1 Mutant Human iPSC Neurons Reveals Shared Endosomal Abnormalities Mediated by APP β-CTFs, Not Aβ

4. Full recovery of the Alzheimer’s disease phenotype by gain of function of vacuolar protein sorting 35

5. Stabilizing the Retromer Complex in a Human Stem Cell Model of Alzheimer’s Disease Reduces TAU Phosphorylation Independently of Amyloid Precursor Protein

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