Cellular prion protein acts as mediator of amyloid beta uptake by caveolin-1 causing cellular dysfunctions in vitro and in vivo,Alzheimer's & Dementia

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Cellular prion protein acts as mediator of amyloid beta uptake by caveolin-1 causing cellular dysfunctions in vitro and in vivo
Alzheimer's & Dementia ( IF 13.0 ) Pub Date : 2024-08-30 , DOI: 10.1002/alz.14120
Angela da Silva Correia ₁ , Matthias Schmitz ₁ , Anna-Lisa Fischer ₁ , Susana da Silva Correia ₁ , Franco L Simonetti ₂ , Gesine Saher ₃ , Roberto Goya-Maldonado ₄ , Amandeep Singh Arora ₅ , Andre Fischer _{6,

7} , Tiago F Outeiro _{8,

9,

10,

11} , Inga Zerr ₁

Affiliation

Department of Neurology, University Medical Center and the German Center for Neurodegenerative Diseases (DZNE), Georg-August University, Goettingen, Germany.
Fundación Instituto Leloir, Buenos Aires, Argentina.
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Goettingen, Germany.
Laboratory of Systems Neuroscience and Imaging in Psychiatry (SNIP-Lab), Department of Psychiatry and Psychotherapy, University Medical Center Goettingen (UMG), Goettingen, Germany.
Texas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Department of Psychiatry and Psychotherapy, University Medical Center Goettingen, Goettingen, Germany.
Department for Systems Medicine and Epigenetics in Neurodegenerative Diseases, German Center for Neurodegenerative Diseases (DZNE) Goettingen, Goettingen, Germany.
Department of Experimental Neurodegeneration, Center for Nanoscale Microscopy and Molecular Physiology of the Brain, Center for Biostructural Imaging of Neurodegeneration, University Medical Center Goettingen, Goettingen, Germany.
Max Planck Institute for Multidisciplinary Sciences, Goettingen, Germany.
Translational and Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle, UK.
Scientific employee with an honorary contract at Deutsches Zentrum für Neurodegenerative Erkrankungen (DZNE), Goettingen, Germany.

Cellular prion protein (PrP^C) was implicated in amyloid beta (Aβ)-induced toxicity in Alzheimer's disease (AD), but the precise molecular mechanisms involved in this process are unclear.

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