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Different α-synuclein prion strains cause dementia with Lewy bodies and multiple system atrophy.
Ayers, Jacob I; Lee, Joanne; Monteiro, Octovia; Woerman, Amanda L; Lazar, Ann A; Condello, Carlo; Paras, Nick A; Prusiner, Stanley B.
Afiliação
  • Ayers JI; Institute for Neurodegenerative Diseases, Weill Institute for Neurosciences, University of California, San Francisco, CA 94158; jacob.ayers@ucsf.edu stanley.prusiner@ucsf.edu.
  • Lee J; Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, CA 94158.
  • Monteiro O; Institute for Neurodegenerative Diseases, Weill Institute for Neurosciences, University of California, San Francisco, CA 94158.
  • Woerman AL; Institute for Neurodegenerative Diseases, Weill Institute for Neurosciences, University of California, San Francisco, CA 94158.
  • Lazar AA; Institute for Neurodegenerative Diseases, Weill Institute for Neurosciences, University of California, San Francisco, CA 94158.
  • Condello C; Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, CA 94158.
  • Paras NA; Division of Biostatistics, University of California, San Francisco, CA 94158.
  • Prusiner SB; Division of Oral Epidemiology and Dental Public Health, University of California, San Francisco, CA 94143.
Proc Natl Acad Sci U S A ; 119(6)2022 02 08.
Article em En | MEDLINE | ID: mdl-35115402
The α-synuclein protein can adopt several different conformations that cause neurodegeneration. Different α-synuclein conformers cause at least three distinct α-synucleinopathies: multiple system atrophy (MSA), dementia with Lewy bodies (DLB), and Parkinson's disease (PD). In earlier studies, we transmitted MSA to transgenic (Tg) mice and cultured HEK cells both expressing mutant α-synuclein (A53T) but not to cells expressing α-synuclein (E46K). Now, we report that DLB is caused by a strain of α-synuclein prions that is distinct from MSA. Using cultured HEK cells expressing mutant α-synuclein (E46K), we found that DLB prions could be transmitted to these HEK cells. Our results argue that a third strain of α-synuclein prions likely causes PD, but further studies are needed to identify cells and/or Tg mice that express a mutant α-synuclein protein that is permissive for PD prion replication. Our findings suggest that other α-synuclein mutants should give further insights into α-synuclein prion replication, strain formation, and disease pathogenesis, all of which are likely required to discover effective drugs for the treatment of PD as well as the other α-synucleinopathies.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Príons / Atrofia de Múltiplos Sistemas / Doença por Corpos de Lewy / Demência / Alfa-Sinucleína Tipo de estudo: Prognostic_studies Limite: Aged / Female / Humans / Male / Middle aged Idioma: En Revista: Proc Natl Acad Sci U S A Ano de publicação: 2022 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Príons / Atrofia de Múltiplos Sistemas / Doença por Corpos de Lewy / Demência / Alfa-Sinucleína Tipo de estudo: Prognostic_studies Limite: Aged / Female / Humans / Male / Middle aged Idioma: En Revista: Proc Natl Acad Sci U S A Ano de publicação: 2022 Tipo de documento: Article