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Oezdemir, I.

Publications and source records attributed to Oezdemir, I..

2 recordsLinked to original sources

Ischemic stroke induces persistent alteration to brain stromal progenitor cells linked to chronic vascular dysfunction

Fibrotic scar formation after stroke serves a dual role: while essential for providing structural support during post-ischemic recovery, excessive fibrosis in the chronic phase of stroke impairs regenerative processes including axonal regrowth and neovascularization. The temporal dynamics of fibrosis are critical determinants of functional outcomes, as the balance between protective scarring and regenerative capacity differs across distinct stroke phases. Consequently, strategic modulation of fibrotic processes to preserve regenerative potential represents a promising therapeutic approach in stroke recovery. To understand the cellular mechanisms underlying this fibrotic response, we investigated stromal progenitor cell composition in the post-stroke brain. The vast majority of stromal progenitor cells (SPCs) are pericytes, with minorities comprising perivascular fibroblasts (PVFs) and vascular smooth muscle cells. We demonstrate that ischemic stroke drives a long-term shift in this composition, characterized by sustained expansion of the PVF population and excessive laminin deposition in the peri-infarct region, effects that persist for at least six months post-stroke. Single-cell RNA sequencing revealed sustained transcriptional and compositional alterations in the SPC population throughout chronic post-stroke phase, driven by AP-1-mediated signaling via TNF in both PVFs and pericytes. These changes correlate with long-term vasomotor dysfunction and capillary constriction in the peri-infarct region at six weeks post-stroke. Ischemic stroke drives aberrant, persistent PVF accumulation at the capillary bed with implications for post-stroke cerebrovascular dysfunction and recurrent stroke. Taken together, these findings reveal that ischemic stroke drives an aberrant long-term mis-localization of PVFs to the capillary bed that may have clinically-relevant implications for post-stroke cerebrovascular function as well as potential ramifications for recurrent stroke.

neuroscience↗

Activating task relevant prior knowledge increases active information storage in content specific brain areas

Predictive coding suggests that the brain infers the causes of its sensations by combining sensory evidence with internal predictions based on available prior knowledge. However, the neurophysiological correlates of (pre-)activated prior knowledge serving these predictions are still unknown. Based on the idea that such pre-activated prior knowledge must be maintained until needed we measured the amount of maintained information in neural signals via the active information storage (AIS) measure. AIS was calculated on whole-brain beamformer-reconstructed source time-courses from magnetoencephalography (MEG) recordings of 52 human subjects during the baseline of a Mooney face/house detection task. Pre-activation of prior knowledge for faces showed as alpha- and beta-band related AIS increases in content specific areas; these AIS increases were behaviourally relevant in brain area FFA. Further, AIS allowed decoding of the cued category on a trial-by-trial basis. Moreover, top-down transfer of predictions estimated by transfer entropy was associated with beta frequencies. Our results support accounts that activated prior knowledge and the corresponding predictions are signalled in low-frequency activity (<30 Hz).\n\nSignificance statementOur perception is not only determined by the information our eyes/retina and other sensory organs receive from the outside world, but strongly depends also on information already present in our brains like prior knowledge about specific situations or objects. A currently popular theory in neuroscience, predictive coding theory, suggests that this prior knowledge is used by the brain to form internal predictions about upcoming sensory information. However, neurophysiological evidence for this hypothesis is rare - mostly because this kind of evidence requires making strong a-priori assumptions about the specific predictions the brain makes and the brain areas involved. Using a novel, assumption-free approach we find that face-related prior knowledge and the derived predictions are represented and transferred in low-frequency brain activity.

neuroscience↗