Biology subjects

Schaefer, J. K.

Publications and source records attributed to Schaefer, J. K..

3 recordsLinked to original sources

bioRxiv2026

Action Sequences Structure Human Memory Reactivation

Episodic memory formation is not a passive process but emerges from sequences of actions through which we engage with our environment. Yet, how these action sequences interact with the neural dynamics underlying human memory formation and retrieval remains poorly understood. Here, we investigated whether coordinated gaze shifts, one of the major exploratory actions in humans, structure the reactivation of memories. Participants learned multiple action sequences by pairing images with distinct real-world gaze shifts while we simultaneously recorded EEG and motion tracking data. During subsequent retrieval, the recalled gaze sequences acted as a direct behavioral readout of memory performance. Representational similarity analyses revealed that the reactivation of image memories was precisely timed to recalled gaze shifts within each sequence. Crucially, only correctly executed, but not incorrectly executed gaze shifts elicited significant reactivation of the corresponding image class, directly linking neural reactivation to retrieval success. These findings suggest that exploratory actions are fundamental components of episodic memories, not incidental accompaniments: self-initiated movements can serve as temporal anchors of memory reactivation that predict retrieval success. By investigating memory through natural behavior, our work provides an ecologically grounded perspective on human cognition, revealing that species-typical actions such as gaze shifts are essential to, rather than obstacles for, understanding memorys neural basis.

neuroscience↗

bioRxiv2023

Mapping Pathways to Neuronal Atrophy in Healthy, Mid-aged Adults: From Chronic Stress to Systemic Inflammation to Neurodegeneration?

Growing evidence implicates systemic inflammation in the loss of structural brain integrity in natural ageing and disorder development. Chronic stress and glucocorticoid exposure can potentiate inflammatory processes and have also been linked to neuronal atrophy, particularly in the hippocampus and the human neocortex. To improve understanding of emerging maladaptive interactions between stress and inflammation, this study examined evidence for glucocorticoid- and inflammation-mediated neurodegeneration in healthy mid-aged adults. N=169 healthy adults (mean age = 39.4, 64.5% female) were sampled from the general population in the context of the ReSource Project. Stress, inflammation and neuronal atrophy were quantified using physiological indices of chronic stress (hair cortisol and cortisone concentration), systemic inflammation (interleukin-6, high-sensitive C-reactive protein), the systemic inflammation index (SII), hippocampal volume (HCV) and cortical thickness (CT) in regions of interest. Structural equation models were used to examined evidence for pathways from stress and inflammation to neuronal atrophy. Model fit indices indicated good representation of stress, inflammation, and neurological data through the constructed models (CT model: robust RMSEA = 0.041, robust{chi} 2= 910.90; HCV model: robust RMSEA < 0.001, robust{chi} 2 = 40.95). We replicated typical negative age-cortical thickness associations (Anterior cingulate cortex ({beta} =-0.51, p < .001), Parahippocampal Cortex ({beta} = -0.50, p = .012), Frontal Lobe ({beta} = -0.56, p < .001) and Temporal Lobe ({beta} = -0.61, p < .001). Among inflammatory indices, only the SII was positively associated with hair cortisol as one indicator of chronic stress ({beta} = 0.18, p<.05). Direct and indirect pathways from chronic stress and systemic inflammation to cortical thickness or hippocampal volume were non-significant. We identify the SII as a potential marker of systemic inflammation in human psychobiological studies. More generally, these data suggest that neurophysiological associations found in at-risk populations are not detectable in healthy, mid-aged populations. We conclude that inflammation and glucocorticoid-mediated neurodegeneration may only emerge during advanced ageing and disorder processes and may thus have limited use as early risk markers. Future work should examine these pathways in prospective longitudinal designs, for which the present investigation serves as a baseline.

neuroscience↗

bioRxiv2018

Mercury methylating microbial communities of boreal forest soils

The formation of the potent neurotoxic methylmercury (MeHg) is a microbially mediated process that has raised much concern because MeHg poses threats to wildlife and human health. Since boreal forest soils can be a source of MeHg in aquatic networks, it is crucial to understand the biogeochemical processes involved in the formation of this pollutant. High-throughput sequencing of 16S rRNA and the mercury methyltransferase, hgcA, combined with geochemical characterisation of soils, were used to determine the microbial populations contributing to MeHg formation in forest soils across Sweden. The hgcA sequences obtained were distributed among diverse clades, including Proteobacteria, Firmicutes, and Methanomicrobia, with Deltaproteobacteria, particularly Geobacteraceae, dominating the libraries across all soils examined. Our results also suggest that MeHg formation is linked to the composition of also non-mercury methylating bacterial communities, likely providing growth substrate (e.g. acetate) for the hgcA-carrying microorganisms responsible for the actual methylation process. While previous research focused on mercury methylating microbial communities of wetlands, this study provides some first insights into the diversity of mercury methylating microorganisms in boreal forest soils.\n\nImportanceDespite a global state of awareness that mercury, and methylmercury in particular, is a neurotoxin that millions of people continue to be exposed to, there are sizable gaps in our fundamental understanding of the processes and organisms involved in methylmercury formation. In the present study we shed light on the diversity of the microorganisms responsible for methylmercury formation in boreal forest soils. All the microorganisms identified have a relevant role on the processing of organic matter in soils. Moreover, our results show that the formation of methylation formation is not only linked to mercury methylating microorganisms but also to the presence of non-mercury methylating bacterial communities that contribute to methylmercury formation by the appropriate substrate to the microorganisms responsible for the actual methylation process. This study improves current knowledge on the diversity of organisms involved in methylmercury formation in soils.

microbiology↗