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Neurodegeneration of the left supramarginal gyrus induces compensatory neural changes during phonological decisions
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Poster D39 in Poster Session D, Wednesday, October 25, 4:45 - 6:30 pm CEST, Espace Vieux-Port
Eduardo Europa1, Andrea Gajardo-Vidal2, Stephen M. Wilson3, Maria Luisa Mandelli4, Giovanni Battistella5,6, Heather R. Dial7, Stephanie M. Grasso8, Lisa D. Wauters8, Rachel Tessmer8, Carly Millanski8, Buddhika Ratnasiri4, Rian Bogley4, Zachary Miller4, Maria Luisa Gorno-Tempini4, Maya Henry8, Diego L. Lorca-Pula9; 1San Jose State University, 2Universidad del Desarrollo, 3University of Queensland, 4University of California, San Francisco, 5Massachusetts Eye and Ear Infirmary, 6Harvard Medical School, 7University of Houston, 8University of Texas at Austin, 9Universidad de Concepción
*BACKGROUND: Previous functional neuroimaging studies have consistently indicated that the left supramarginal gyrus (LSMG) is part of the core phonological network with observed increases in LSMG activation during phonological relative to semantic decisions. Moreover, its causal involvement in phonological processing has been ascertained in studies demonstrating selective disruption of phonological decisions following inhibitory transcranial magnetic stimulation over LSMG. Inhibition of LSMG activity during phonological decisions has also been shown to induce transient neural changes in remote brain regions. These findings motivated us to examine whether LSMG atrophy induces compensatory neural changes during phonological decisions in logopenic variant primary progressive aphasia (lvPPA), a neurodegenerative syndrome characterized by progressive loss of phonological abilities. *METHODS: All study participants completed three fMRI tasks in which they decided whether (i) two pseudowords rhymed (phon), (ii) two words were related in meaning (sem), or (iii) two false font strings were identical (baseline). First, we identified a functionally defined LSMG region-of-interest (ROI) by comparing activation during phon>sem in a group of 16 healthy controls. Second, we segregated 16 mild-moderate lvPPA participants into two groups according to degree of tissue loss in the LSMG-ROI: (1) those with greater than 50% damage (lvPPA-LSMG-atrophy group, n=6; mean LSMG-ROI damage=74%); and (2) those with less than 50% damage (lvPPA-control group, n=10; mean LSMG-ROI damage=18%). *RESULTS: All groups performed significantly above chance on all tasks. As expected, lvPPA participants performed less accurately than healthy controls on phon and sem tasks. An fMRI conjunction analysis of phon>baseline across groups highlighted that lvPPA-LSMG-atrophy participants primarily recruited the left frontal part of the normal phonological network, although other areas such as the posterior LSMG were also activated. Adjacent to the normal phonological network, lvPPA-LSMG-atrophy participants showed increased activation in a region within the left anterior middle frontal gyrus (LaMFG-ROI) relative to healthy controls and lvPPA-control participants. Furthermore, this LaMFG-ROI was more engaged during phon>sem in the lvPPA-LSMG-atrophy participants only, resulting in a significant group by task interaction. Interestingly, we found greater LaMFG-ROI activation with increasing LSMG-ROI atrophy. To dismiss the possibility that greater LaMFG-ROI activation in lvPPA-LSMG-atrophy participants may exclusively be driven by increased cognitive effort during inaccurate phon responses, we carried out a post-hoc analysis where accurate and inaccurate responses were modeled separately. Our post-hoc analysis revealed a significant increase in LaMFG-ROI activation in lvPPA-LSMG-atrophy participants during accurate phon trials relative to (i) accurate baseline trials and (ii) accurate sem trials. *CONCLUSIONS: When making phonological decisions, lvPPA participants with LSMG atrophy recruited a substantial portion of the normal phonological network. Outside this network, lvPPA-LSMG-atrophy participants showed enhanced activation within the LaMFG relative to healthy controls. This effect was both lesion- (lvPPA-LSMG-atrophy>lvPPA-control) and task-specific (phon>sem). We hypothesize that the LaMFG may play a compensatory role by exerting top-down control over the phonological computations carried out in LSMG, which have become noisier due to the disruptive effect of neurodegeneration. Future studies should investigate whether non-invasive neurostimulation of LaMFG improves phonological processing in the context of LSMG neurodegeneration.
Topic Areas: Disorders: Acquired, Phonology