Co-expression of APP/PS1 disrupts the distribution of brain lesions in a synucleinopathy transgenic mouse model (M83)

Acta Neuropathol. 2022 Apr;143(4):527-529. doi: 10.1007/s00401-022-02410-x. Epub 2022 Mar 7.

Authors

Thierry Baron¹, Jean-Noël Arsac², Jérémy Verchère², Habiba Tlili², Claire Aufauvre², Dominique Bétemps²

Affiliations

¹ ANSES-Laboratoire de Lyon (French Agency for Food, Environmental and Occupational Health & Safety), University of Lyon, 31 avenue Tony Garnier, 69364, Lyon, Cedex 7, France. thierry.baron@anses.fr.
² ANSES-Laboratoire de Lyon (French Agency for Food, Environmental and Occupational Health & Safety), University of Lyon, 31 avenue Tony Garnier, 69364, Lyon, Cedex 7, France.

PMID: 35257220
DOI: 10.1007/s00401-022-02410-x

No abstract available

Publication types

Letter

MeSH terms

Alzheimer Disease* / genetics
Amyloid beta-Peptides / genetics
Amyloid beta-Peptides / metabolism
Amyloid beta-Protein Precursor / genetics
Animals
Brain / metabolism
Disease Models, Animal
Mice
Mice, Transgenic
Presenilin-1 / genetics
Presenilin-1 / metabolism
Synucleinopathies* / genetics

Substances

Amyloid beta-Peptides
Amyloid beta-Protein Precursor
Presenilin-1