Biology subjects

Federspiel, A.

Publications and source records attributed to Federspiel, A..

3 recordsLinked to original sources

bioRxiv2025

Neural Traces of Forgotten Memories Persist in Humans and are Behaviorally Relevant

For a long time, forgetting has been taken as the dissipation of the neural memory traces (engrams). However, recent engram research in mice suggests that the engrams of forgotten memories do persist. This raises the question of whether engrams underlying human episodic memories also persist despite forgetting? And do forgotten memories influence human behavior implicitly? To address these questions, we used high-resolution functional magnetic resonance imaging at 7 Tesla to map the fate of 96 associative memories at the systems level from learning to a 30-minute and onward to a 24-hour memory test. Upon each retrieval attempt, participants indicated whether they remembered or forgot the memory. Univariate and multivariate analyses of the functional brain data revealed that the engrams of forgotten memories remain implemented in the episodic memory network and continue to influence the accuracy of guessing responses at the memory test. Overnight, the engrams of forgotten memories became implemented more deeply within bilateral hippocampus, while consciously accessible memories were neocorticalized overnight. The engrams of both consciously accessible and inaccessible (forgotten) memories shifted from the 30-minute to the 24-hour memory test within the right hippocampus and anterior cingulate gyrus as evidenced by the occurrence of pattern dissimilarities that supported correct retrieval responses at 24 hours. Hence, forgotten human episodic memories remain implemented in the episodic memory system and continue to influence decisions.

neuroscience↗

bioRxiv2020

Altered central pain processing in fibromyalgia - a multimodal neuroimaging case-control study using arterial spin labelling

Fibromyalgia is characterized by chronic pain and a striking discrepancy between objective signs of tissue damage and severity of pain. Function and structural alterations in brain areas involved in pain processing may explain this feature. Previous case-control studies in fibromyalgia focused on acute pain processing using experimentally-evoked pain paradigms. Yet, these studies do not allow conclusions about chronic, stimulus-independent pain. Resting-state cerebral blood flow (rsCBF) acquired by arterial spin labelling (ASL) may be a more accurate marker for chronic pain. The objective was to integrate four different functional and structural neuroimaging markers to evaluate the neural correlate of chronic, stimulus-independent pain using a resting-state paradigm. In line with the pathophysiological concept of enhanced central pain processing we hypothesized that rsCBF is increased in fibromyalgia in areas involved in processing of acute pain. We performed an age matched case-control study of 32 female fibromyalgia patients and 32 pain-free controls and calculated group-differences in rsCBF, resting state functional connectivity, grey matter density and cortical thickness using whole-brain and region of interest analyses. We adjusted all analyses for depression and anxiety. As centrally acting drugs are likely to interfere with neuroimaging markers, we performed a subgroup analysis limited to patients not taking such drugs. We found no differences between cases and control in rsCBF of the thalamus, the basal ganglia, the insula, the somatosensory cortex, the prefrontal cortex, the anterior cingulum and supplementary motor area as brain previously identified to be involved in acute processing in fibromyalgia. The results remained robust across all four neuroimaging markers and when limiting the study population to patients not taking centrally acting drugs and matched controls. In conclusion, we found no evidence for functional or structural alterations in brain areas involved in pain processing in fibromyalgia that could reflect neural correlates of chronic stimulus-independent pain.

neuroscience↗

bioRxiv2017

Glucocorticoids change neural decoding in the middle cingulate cortex accompanied by a reduction of subjective fear in patients with spider phobia

Glucocorticoids--stress hormones released from the adrenal cortex--reduce phobic fear in anxiety disorders and enhance psychotherapy, possibly by reducing the retrieval of fear memories and enhancing the consolidation of new corrective memories. Glucocorticoid signaling in the basolateral amygdala can influence connected fear and memory-related cortical regions, but this is not fully understood. Previous studies investigated specific pathways moderated by glucocorticoids, for example, visual-temporal pathways; however, these analyses were limited to a-priori selected regions. Here, we performed whole-brain pattern analysis to localize phobic stimulus decoding related to the fear-reducing effect of glucocorticoids. We reanalyzed functional magnetic resonance imaging (fMRI) data from a previously published study with spider-phobic patients and healthy controls. The patients received either glucocorticoids or a placebo treatment before the exposure to spider images. There was moderate evidence that patients with phobia had higher decoding of phobic content in the anterior cingulate cortex (ACC) and the left and right anterior insula compared to controls. Decoding in the ACC and the right insula showed strong evidence for correlation with experienced fear. Patients with cortisol reported a reduction of fear by 10-13%; however, there was only weak evidence for changes in neural decoding compared to placebo which was found in the precuneus, the opercular cortex, and the left cerebellum.

neuroscience↗