Work

Gga3 deletion and a GGA3 rare variant associated with late onset Alzheimer’s disease trigger BACE1 accumulation in axonal swellings

Year: 2020

Type: article

Abstract: deletion exacerbates axonal dystrophies in a mouse model of AD before β-amyloid (Aβ) deposition. Our study strongly supports a role for GGA3 in AD pathogenesis, where GGA3 loss of function triggers BACE1 axonal accumulation independently of extracellular Aβ, and initiates a cascade of events leading to the axonal damage distinctive of the early stage of AD.

Source: Science Translational Medicine

DOI: 10.1126/scitranslmed.aba1871

Authors: Selene Lomoio, Rachel Willen, WonHee Kim, Kevin Z. Ho, Edward K. Robinson, Dmitry Prokopenko, Matthew E. Kennedy, Rudolph E. Tanzi, Giuseppina Tesco

Institutions: Tufts University, Harvard University, Massachusetts General Hospital, Merck & Co., Inc., Rahway, NJ, USA (United States)

Language: English

Topic: Alzheimer's disease research and treatments

Subfield: Physiology

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: green

Funders: BrightFocus Foundation, Cure Alzheimer's Fund, National Institute on Aging, National Heart, Lung, and Blood Institute, National Institute of General Medical Sciences

Awards: Building Diversity in Biomedical Sciences, BACE1 trafficking and degradation in Alzheimer’s disease, Tufts Post-Baccalaureate Research Education Program

OpenAlex ID: W3100220025

FWCI: 1.503

Cites: 64

Cited by: 23

Related to: 10