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Bonelli, S.

Publications and source records attributed to Bonelli, S..

4 recordsLinked to original sources

Beyond the Resection: Surgical White Matter Disruption alters Non-Resected Brain Anatomy

Resective neurosurgery is a cornerstone treatment for many neurological conditions. Although traditionally viewed as localised procedure, increasing evidence from advanced magnetic resonance imaging (MRI) shows that also non-resected anatomy can degenerate following surgery. The relationship between local tissue removal and these postoperative changes remains thus far speculative. Here, we investigate the hypothesis that degenerative changes to surgically preserved grey and white matter are mediated by transneuronal degeneration, a deterioration of intact neuronal populations due to lost axonal input. Using a robust structural and diffusion MRI framework, we first identify widespread postoperative atrophy: pronounced cortical thickness decreases near the resection, and extensive white matter impairments across the ipsilateral hemisphere. Importantly, we then link these alterations to surgical white matter disruption, revealing a sequential network atrophy following neurosurgery. Beyond degenerative effects, we also demonstrate often reported structural network reorganisations as an artefact of image processing, indicating limited capacity for macroscale plasticity post-resection. Key PointsO_LIResective neurosurgery can lead to postoperative atrophy of non-resected grey and white matter. Utilising a robust longitudinal neuroimaging framework, we evaluate these changes as consequences of transneuronal degeneration, demonstrating a sequential atrophy of brain anatomy following the loss of surgically disrupted white matter. C_LIO_LIThe majority of severed connections projected to atrophic cortices near the resection, indicating them to be short association fibers. Consecutive white matter atrophy however affected extensive ipsilateral pathways, highlighting a cascading network effect of resective brain surgery. C_LIO_LIWe did not find evidence to support often reported structural reorganisations of large-scale brain networks post-resection. Yet, we demonstrate that evidence typically interpreted as such can be replicated when using non-robust reconstruction methods. C_LI

neuroscience↗

The interplay of climate change, urbanization, and species traits shapes European butterfly population trends

Species populations naturally fluctuate, yet long-term trend analysis can reveal patterns of success, decline, or stability under global change pressures. While responses to climate change are well-documented, its synergy with another major global driver, urbanization, remains understudied. Here, we analyzed long-term monitoring data from over 8,400 populations of 145 butterfly species across Europe, representing a high diversity of species traits, to assess population trends in response to climate change and urbanization. We examined how population responses vary between urban and rural contexts, providing insights into the influence of site-specific conditions. Climate warming was associated with population declines, which were more pronounced in urban areas. The effect of precipitation varied between environments: increases in precipitation generally benefited populations in rural areas but had detrimental effects in urban ones. Aridity consistently drove population declines across environments, with slightly stronger effects in urban areas. Species with colder climatic niches declined the most in response to warming, increased aridity, and reduced precipitation, while trophic specialists were particularly vulnerable to aridity and precipitation changes in urban environments. Although increasing urbanization did not explain overall population trends, its effects became evident when considering species traits, with certain traits being more vulnerable to urbanization. Specifically, species with narrow climatic niches declined the most in response to urbanization in rural areas, while those and larger body sizes decline the most in urban environments. Our findings highlight the complex interplay between environmental change, landscape context, and species traits in shaping biodiversity outcomes. Importantly, our results suggest that urbanization generally amplifies the impact of climate change on insect population trends.

ecology↗

Contrasting genetic differentiation of urban and rural populations of two grassland lepidopterans across Europe

Urbanisation is transforming environments globally. The altered abiotic conditions and biotic interactions in urban habitats impose divergent selection pressures on urban versus rural populations, while genetic drift may also be significant in typically small urban populations. A key question in urban evolution concerns the origin and spread of urban genotypes. Examples exist of both single and multiple origins of urban genotypes, but these have proven difficult to generalize. Here, we address genetic differentiation among urban populations, among rural populations, and between urban and rural populations. We conducted an extensive population genomic double digest restriction-site associated DNA sequencing analysis of two non-model grassland lepidopterans, Coenonympha pamphilus and Chiasmia clathrata, across Europe. The genetic population structures of the study species were strikingly different: Co. pamphilus showed strong population differentiation, while this was almost absent in Ch. clathrata, which instead showed signs of high current and past gene flow among populations. Results of Co. pamphilus are consistent with multiple origins of urban populations, and multiple origins seem plausible also in Ch. clathrata. These results suggest that past and large-scale population dynamics need to be integrated into urban evolution research, because population history affects urban evolutionary dynamics.

evolutionary biology↗

Uncovering the ligandome of low-density lipoprotein receptor-related protein 1 in cartilage: a top-down approach to identify therapeutic targets

The low-density lipoprotein receptor-related protein 1 (LRP1) is a cell-surface receptor ubiquitously expressed in adult tissues. It plays tissue-specific physiological roles by mediating endocytosis of a diverse range of extracellular molecules. Dysregulation of LRP1 is involved in multiple conditions including Alzheimers disease, atherosclerosis and osteoarthritis (OA). However, little information is available about the specific ligand profile (ligandome) for each tissue, which would lead to better understanding of its role in disease states. Here, we investigated adult articular cartilage where impaired LRP1-mediated endocytosis leads to tissue destruction. We used a top-down approach involving analysis of human chondrocyte secretome, direct binding assays and validation in LRP1-deficient fibroblasts, as well as a novel Lrp1 conditional knockout (KO) mouse model. We found that inhibition of LRP1-mediated endocytosis results in cell death, alteration of the entire secretome and transcriptional modulations in human chondrocytes. We have identified more than 50 novel ligand candidates and confirmed direct LRP1 binding of HGFAC, HMGB1, HMGB2, CEMIP, SLIT2, ADAMTS1, IGFBP7, SPARC and LIF. Our in vitro endocytosis assay revealed the correlation of their affinity for LRP1 and the rate of endocytosis. Moreover, a conditional LRP1 KO mouse model demonstrated a critical role of LRP1 in regulating the high-affinity ligands in cartilage in vivo. This systematic approach revealed the extent of the chondrocyte LRP1 ligandome and identified potential novel therapeutic targets for OA.

cell biology↗