Focal temporal pole atrophy and network degeneration in semantic variant primary progressive aphasia


Por: Collins, JA, Montal, V, Hochberg, D, Quimby, M, Mandelli, ML, Makris, N, Seeley, WW, Gorno-Tempini, ML, Dickerson, BC

Publicada: 1 feb 2017
Resumen:
A wealth of neuroimaging research has associated semantic variant primary progressive aphasia with distributed cortical atrophy that is most prominent in the left anterior temporal cortex; however, there is little consensus regarding which region within the anterior temporal cortex is most prominently damaged, which may indicate the putative origin of neurodegeneration. In this study, we localized the most prominent and consistent region of atrophy in semantic variant primary progressive aphasia using cortical thickness analysis in two independent patient samples (n = 16 and 28, respectively) relative to age-matched controls (n = 30). Across both samples the point of maximal atrophy was located in the same region of the left temporal pole. This same region was the point of maximal atrophy in 100% of individual patients in both semantic variant primary progressive aphasia samples. Using resting state functional connectivity in healthy young adults (n = 89), we showed that the seed region derived from the semantic variant primary progressive aphasia analysis was strongly connected with a large-scale network that closely resembled the distributed atrophy pattern in semantic variant primary progressive aphasia. In both patient samples, the magnitude of atrophy within a brain region was predicted by that region's strength of functional connectivity to the temporopolar seed region in healthy adults. These findings suggest that cortical atrophy in semantic variant primary progressive aphasia may follow connectional pathways within a large-scale network that converges on the temporal pole.

Filiaciones:
Collins, JA:
 Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurol, Charlestown, MA USA

Montal, V:
 Univ Autonoma Barcelona, Inst Invest Biomed St Pau, Dept Neurol, Hosp St Pau, Barcelona, Spain

Hochberg, D:
 Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurol, Charlestown, MA USA

Quimby, M:
 Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurol, Charlestown, MA USA

Mandelli, ML:
 Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA

Makris, N:
 Harvard Med Sch, Massachusetts Gen Hosp, Dept Psychiat, Charlestown, MA USA

Seeley, WW:
 Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA

 Univ Calif San Francisco, Dept Pathol, San Francisco, CA 94140 USA

Gorno-Tempini, ML:
 Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA

Dickerson, BC:
 Harvard Med Sch, Massachusetts Gen Hosp, Dept Neurol, Charlestown, MA USA
ISSN: 00068950





BRAIN
Editorial
OXFORD UNIV PRESS, GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND, Reino Unido
Tipo de documento: Article
Volumen: 140 Número:
Páginas: 457-471
WOS Id: 000397315900027
ID de PubMed: 28040670
imagen Green Published, Bronze

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