To determine whether the alterations in p38α and p38γ observed in DLB brains also occurred in transgenic animal models of α-synucleinopathies, we investigated the distribution of α-syn and these p38 isoforms in mice overexpressing human wild type α-syn under the Thy-1 promoter (α-syn Tg) and their non-transgenic littermates (non-Tg). This evidence concerns the gene THY1 and Lewy body dementia.