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Article type: Short Communication
Authors: López-González, Irenea; 1 | Palmeira, Andreb; 1 | Aso, Estera | Carmona, Margaritaa | Fernandez, Lianab; * | Ferrer, Isidroa; c; d; *
Affiliations: [a] Institute of Neuropathology, Bellvitge University Hospital-IDIBELL, L’Hospitalet de Llobregat, Barcelona, Spain | [b] Universidade Federal de Ciências da Saúde de Porto Alegre (UFCSPA), Porto Alegre, Brazil | [c] University of Barcelona, L’Hospitalet de Llobregat, Barcelona, Spain | [d] CIBERNED, Instituto Carlos III, Madrid, Spain
Correspondence: [*] Correspondence to: Prof. Isidro Ferrer, Institute of Neuropathology, Service of Anatomic Pathology, Bellvitge University Hospital, c/ Feixa Llarga sn, 08907 L’Hospitalet de Llobregat, Spain. Tel.: +3493 4035808; E-mail: 8082ifa@gmail.com and Prof. Liana Fernandez, Universidade federal de ciências da saúde de Porto Alegre (UFCSPA), Porto Alegre, Brazil. E-mail: llfernandez@plugin.com.br.
Note: [1] These authors contributed equally to this work.
Abstract: FOXP2 is altered in a variety of language disorders. We found reduced mRNA and protein expression of FOXP2 in frontal cortex area 8 in Pick’s disease, and frontotemporal lobar degeneration-tau linked to P301L mutation presenting with language impairment in comparison with age-matched controls and cases with parkinsonian variant progressive supranuclear palsy. Foxp2 mRNA and protein are also reduced with disease progression in the somatosensory cortex in transgenic mice bearing the P301S mutation in MAPT when compared with wild-type littermates. Our findings support the presence of FOXP2 expression abnormalities in sporadic and familial frontotemporal degeneration tauopathies.
Keywords: FOXP2, frontotemporal lobar degeneration, language, Pick’s disease, P301S transgenic mice, tauopathy
DOI: 10.3233/JAD-160274
Journal: Journal of Alzheimer's Disease, vol. 54, no. 2, pp. 471-475, 2016
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