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Krause, P.

Publications and source records attributed to Krause, P..

6 recordsLinked to original sources

Urbanisation drives biodiversity loss, fitness decline and community shifts in cavity-nesting Hymenoptera

Urbanisation is reshaping landscapes worldwide, posing challenges to biodiversity and ecosystem function. Cavity-nesting Hymenoptera, including bees and wasps, deliver vital ecological services but are increasingly vulnerable to urbanisation. In this citizen science-based study, we deployed 286 trap nests across Leipzig and Hamburg (Germany) to investigate how urbanisation and landscape-scale environmental features influence the diversity, community composition, reproductive success, offspring survival and demographic status of these insects. Using Bayesian hierarchical and phylogenetically informed modelling, we found that urbanisation significantly reduced species richness, reproductive output and offspring survival in both guilds, despite stable nesting activity, suggesting potential ecological trap effects. For bees, urbanisation also reduced the probability of nests functioning as demographic sources. Environmental drivers shaped responses in taxon-specific ways: bee richness and survival increased with landscape diversity but declined with fragmentation, while wasp richness and nesting declined with higher temperatures, though survival increased with more green cover. Bee nests were more likely to serve as demographic sources in higher temperatures. Community composition responses also diverged; bee communities shifted via increased species turnover, while wasp assemblages remained relatively stable. Temperature was a major driver of compositional dissimilarity in both groups, whereas landscape diversity was associated with homogenisation in bees and diversification in wasps. Our findings demonstrate that cities filter cavity-nesting Hymenoptera through multiple ecological pathways, highlighting the need for differentiated conservation strategies that consider both habitat structure and taxon-specific responses.

ecology↗

Dynamics of cortico-subthalamic neuronal patterns during dyskinesia in Parkinsons disease

Parkinson patients suffer from levodopa-induced dyskinesia, which occur adversely to chronic dopaminergic treatment. These abnormal involuntary movements can only partly be actively suppressed and affect quality of life. A lowered motor inhibition during hyperdopaminergic states, associated with structural and plasticity changes in the cortico-basal-ganglia motor network, is hypothesized to enable dyskinesia. Oscillatory cortico-subthalamic patterns associated with dyskinesia are proposed as adaptive neuromodulation biomarkers, but their dependence on behavioral states such as dyskinetic movement presence or suppression remains unknown. We studied cortico-subthalamic oscillations in 22 Parkinsons patients during dyskinesia-evoking protocols. We clinically differentiated between non-dyskinetic and dyskinetic periods, and defined movement presence with kinematics, leading to four behavioral states containing rest, voluntary movements, movement suppression during dyskinesia, and dyskinetic movements. Elevated subthalamic theta-activity and attenuated beta-activity was found during both dyskinetic movement suppression and execution, while cortico-subthalamic gamma-activity only increased during dyskinetic movement execution. Subthalamic spectral changes significantly predicted dyskinesia presence, and movement presence significantly affected the predictive performance. A movement-aware classifier enhanced dyskinesia detection based on movement-depending biomarkers containing cortical oscillations and gamma-bands. We propose movement execution during dyskinesia to be a distinct behavioral and neural microstate within a dopamine-depending dyskinetic macrostate, that can enhance dyskinesia classification for adaptive neuromodulation.

neuroscience↗

Differential modulation of movement speed with state-dependent deep brain stimulation in Parkinson's disease

Subthalamic deep brain stimulation (STN-DBS) provides unprecedented spatiotemporal precision for the treatment of Parkinsons disease (PD), allowing for direct real-time state-specific adjustments. Inspired by findings from optogenetic stimulation in mice, we hypothesized that STN-DBS effects on movement speed depend on ongoing movement kinematics that patients exhibit during stimulation. To investigate this hypothesis, we implemented a motor state-dependent closed-loop neurostimulation algorithm, adapting DBS burst delivery to ongoing movement speed in 24 PD patients. We found a stronger anti-bradykinetic effect, raising movement speed to the level of healthy controls, when STN-DBS was applied during fast but not slow movements, while only stimulating 5% of overall movement time. To study underlying brain circuits and neurophysiological mechanisms, we investigated the behavioral effects with MRI connectomics and motor cortex electrocorticography. Finally, we demonstrate that machine learning-based brain signal decoding can be used to predict continuous movement speed for fully embedded state-dependent closed-loop algorithms. Our findings provide novel insights into the state-dependency of invasive neuromodulation, which could inspire advanced state-dependent neurostimulation algorithms for brain disorders.

neuroscience↗

Beyond beta: Aperiodic broadband power reflects Parkinson's disease severity - a multicenter study

Parkinsons disease is linked to increased beta oscillations in the subthalamic nucleus, which correlate with motor symptoms. However, findings across studies have varied. Our standardized analysis of multicenter datasets shows that small sample sizes contributed to these discrepancies--a challenge we address by pooling datasets into one large cohort (n=119). Moving beyond beta power, we disentangled spectral components reflecting distinct neural processes. Combining aperiodic offset, low beta, and low gamma oscillations explained significantly more variance in symptom severity than beta alone. Moreover, interhemispheric within-patient analyses showed that, unlike beta oscillations, aperiodic broadband power-likely reflecting spiking activity-was increased in the more affected hemisphere. These findings identify aperiodic broadband power as a potential biomarker for adaptive deep brain stimulation and provide novel insights into the relationship between subthalamic hyperactivity and motor symptoms in human Parkinsons disease.

neuroscience↗

Shared pathway-specific network mechanisms of dopamine and deep brain stimulation for the treatment of Parkinson's disease

Deep brain stimulation is a brain circuit intervention that can modulate distinct neural pathways for the alleviation of neurological symptoms in patients with brain disorders. In Parkinsons disease, subthalamic deep brain stimulation clinically mimics the effect of dopaminergic drug treatment, but the shared pathway mechanisms on cortex - basal ganglia networks are unknown. To address this critical knowledge gap, we combined fully invasive neural multisite recordings in patients undergoing deep brain stimulation surgery with normative MRI-based whole-brain connectomics. Our findings demonstrate that dopamine and stimulation exert distinct mesoscale effects through modulation of local neural population activity. In contrast, at the macroscale, stimulation mimics dopamine in its suppression of excessive interregional network synchrony associated with indirect and hyperdirect cortex - basal ganglia pathways. Our results provide a better understanding of the circuit mechanisms of dopamine and deep brain stimulation, laying the foundation for advanced closed-loop neurostimulation therapies.

neuroscience↗

Modulating the human functional connectome using deep brain stimulation

Neuroimaging has seen a paradigm shift from a formal description of local activity patterns toward studying distributed brain networks. The recently defined framework of the human connectome allows to globally analyse parts of the brain and their interconnections. Deep brain stimulation (DBS) is an invasive therapy for patients with severe movement disorders aiming to retune abnormal brain network activity by local high frequency stimulation of the basal ganglia. Beyond clinical utility, DBS represents a powerful research platform to study functional connectomics and the modulation of distributed brain networks in the human brain. We acquired resting-state functional MRI in twenty Parkinsons disease (PD) patients with subthalamic DBS switched ON and OFF. An age-matched control cohort of fifteen subjects was acquired from an open data repository. DBS lead placement in the subthalamic nucleus (STN) was localized using a state-of-the art pipeline that involved brain shift correction, multispectral image registration and use of a precise subcortical atlas. Based on a realistic 3D model of the electrode and surrounding anatomy, the amount of local impact of DBS was estimated using a finite element method approach. On a global level, average connectivity increases and decreases throughout the brain were estimated by contrasting ON and OFF DBS scans on a voxel-wise graph comprising eight thousand nodes. Local impact of DBS on the sensorimotor STN explained half the variance in global connectivity increases within the sensorimotor network (R = 0.711, p < 0.001). Moreover, local impact of DBS on the motor STN could explain the degree of how much voxel-wise average brain connectivity normalized toward healthy controls (R = 0.713, p < 0.001). Finally, a network based statistics analysis revealed that DBS attenuated specific couplings that are known to be pathological in PD. Namely, coupling between motor thalamus and sensorimotor cortex was increased and striatal coupling with cerebellum, external pallidum and STN was decreased by DBS. Our results show that rs-fMRI may be acquired in DBS ON and OFF conditions on clinical MRI hardware and that data is useful to gain additional insight into how DBS modulates the functional connectome of the human brain. We demonstrate that effective DBS increases overall connectivity in the motor network, normalizes the network profile toward healthy controls and specifically strengthens thalamo-cortical connectivity while reducing striatal control over basal ganglia and cerebellar structures.

neuroscience↗