Microglial autophagy–associated phagocytosis is essential for recovery from neuroinflammation

Author:

Berglund Rasmus1ORCID,Guerreiro-Cacais Andre Ortlieb1ORCID,Adzemovic Milena Z.1,Zeitelhofer Manuel2,Lund Harald1ORCID,Ewing Ewoud1ORCID,Ruhrmann Sabrina1,Nutma Erik3,Parsa Roham1ORCID,Thessen-Hedreul Melanie1,Amor Sandra34ORCID,Harris Robert A.1ORCID,Olsson Tomas1ORCID,Jagodic Maja1ORCID

Affiliation:

1. Department of Clinical Neuroscience, Karolinska Institutet, Center for Molecular Medicine, Karolinska University Hospital, 171 76 Stockholm, Sweden.

2. Division of Vascular Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, 171 65 Solna, Sweden.

3. Department of Pathology, Amsterdam UMC, Location VUmc, De Boelelaan 1117, 1081 HV Amsterdam, Netherlands.

4. Centre for Neuroscience and Trauma, Blizard Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK.

Abstract

Degradation of tissue debris and recovery from neuroinflammatory disease are impaired in Atg7 -deficient microglia, a process mirrored by aging.

Funder

AstraZeneca

Hjärnfonden

Karolinska Institutet

Knut och Alice Wallenbergs Stiftelse

Stockholms Läns Landsting

Swedish Research Council for Health, Working Life and Welfare

European Union Horizon

Swedish Association for Persons with Neurological Disabilities

Publisher

American Association for the Advancement of Science (AAAS)

Subject

General Medicine,Immunology

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