Biology subjects

Sandberg, C.

Publications and source records attributed to Sandberg, C..

2 recordsLinked to original sources

bioRxiv2026

Iconic Sound-Shape Correspondences in Aphasia

PurposeTo examine speech iconicity for shape in aphasia, we compared iconicity ratings from people with aphasia to those from neurologically intact individuals and evaluated how iconicity relates to phonological and semantic processing profiles in aphasia. MethodEleven people with aphasia and 11 age- and gender-matched neurologically intact participants rated how rounded or pointed 50 auditory pseudowords sounded using a 5-point scale. Ratings from participants with aphasia were compared to predicted iconicity ratings derived from reference ratings from prior work and to ratings from neurologically intact participants. For each participant with aphasia, correlations between individual ratings and predicted ratings were related to measures of phonological and semantic processing. ResultsRatings from people with aphasia were significantly correlated with both the predicted ratings and the ratings from neurologically intact participants. The strength of the correlation between individual ratings and predicted ratings did not differ significantly between groups, although there was a trend toward weaker correlations in the aphasia group. There were indications that greater language impairment was associated with greater disruption of iconicity ratings; in particular, deficits in phonological segmentation and semantic processing were associated with reduced sensitivity to shape iconicity. ConclusionThese findings suggest that sensitivity to shape iconicity is preserved in individuals with aphasia to varying degrees. The specific nature of language impairment appears to play an important role in determining iconicity processing in aphasia.

neuroscience↗

bioRxiv2024

Integrated stress response associated with dark microglia promotes microglial lipogenesis and contributes to neurodegeneration

Microglia, the brains primary resident immune cells, are a heterogeneous population and can assume phenotypes with diverse functional outcomes on brain homeostasis. In Alzheimers disease (AD), where microglia are a leading causal cell type, microglia subsets with protective functions have been well characterized. Yet, the identity of microglia subsets that drive neurodegeneration remains unresolved. Here, we identify a neurodegenerative microglia phenotype that is characterized by a conserved stress signaling pathway, the integrated stress response (ISR). Using mouse models to activate or inhibit ISR in microglia, we show that ISR underlies the ultrastructurally distinct "dark" microglia subset linked to pathological synapse loss. Inducing microglial ISR in murine AD models exacerbates neurodegenerative pathologies, such as Tau pathology and synaptic terminal loss. Conversely, inhibiting microglial ISR in AD models ameliorates these pathologies. Mechanistically, we present evidence that ISR promotes the secretion of toxic long-chain lipids that impair neuron and oligodendrocyte homeostasis in vitro. Accordingly, small molecule-based inhibition of lipid synthesis in AD models ameliorates synaptic terminal loss. Our results demonstrate that activation of ISR within microglia represents a novel pathway contributing to neurodegeneration and suggest that this may be sustained, at least in part, by the secretion of long-chain lipids from ISR-activated microglia.

neuroscience↗