Biology subjects

Bondolfi, G.

Publications and source records attributed to Bondolfi, G..

3 recordsLinked to original sources

bioRxiv2026

The anger-insula-body link in heart arrhythmias

Anger is a well-known risk factor in cardiovascular diseases (CVDs) since it triggers a sympathetic hyperactivity of peripheral autonomic nervous system (ANS). As our previous findings showed, facing an angry situation instead of a joyful one elicits in healthy participants an affective engagement that involved mainly the insular reactivity and its connectivity. On the other hand, stimulating the insula, the key neural hub of the cardiovascular brain, can induce cardiac arrhythmias. Unfortunately, still little is known about the interplay between the anger and the insula as the underlying emotional-brain-body link that can trigger or precipitate a series of neurogenic cardiac events in CVDs patients. To address this question, we employed a multimodal method combining neuroimaging, behavioral and blood data to gain a more complete picture of the insula activity and its connectivity in patients with different types of heart arrhythmias. The present findings show a greater generalized involvement of the bilateral posterior insulae in the patients group both when facing angry context and squeezing the handgrip device, suggesting an automatic engagement of the sympathetic nervous system/SNS. Moreover, the bilateral insulae were functionally coupled with the bilateral lateral ventricles selectively under angry conditions, suggesting an insular role in glymphatic dysfunction and CSF dynamics due to the neurovascular coupling. Clearly, understanding this anger-insula-heart link may factually contribute to lower the probability of adverse cardiac outcomes in orienting the necessary treatment of the person, taking into account the emotion-related cardiovascular pathologies and the psychological health.

neuroscience↗

bioRxiv2026

Hippocampal-somatomotor coactivation and perceived benefit following Mindfulness-Based Cognitive Therapy for Life in healthcare students: An exploratory randomized study

Mindfulness-based interventions are known to enhance emotion regulation and stress management, yet their neural mechanisms remain incompletely understood. Effective coping strategies for emotion regulation and stress management would be particularly beneficial for healthcare students, frequently exposed to highly stressful situations. Based on prior work implicating hippocampal-somatomotor dynamics in emotion regulation, we tested whether Mindfulness-Based Cognitive Therapy for Life (MBCT-L) modulates hippocampal micro-coactivation patterns (CAPs) in healthcare students. In a randomized controlled study including 161 healthcare students, 57 participants (39 females; mean age: 23+/-5 years old) completed resting-state fMRI before and after the 8-weeks intervention and were allocated to MBCT-L (N = 24) or a no-intervention control (N = 33) condition. Hippocampus-seeded CAPs analysis identified six recurrent patterns, including a somatomotor network. MBCT-L improved self-reported mindfulness, but no significant Group*Time interaction for hippocampus-somatomotor coactivation or resting physiological measures was found. In the MBCT-L group, higher hippocampus-somatomotor co-activity was associated with higher perceived importance of the intervention, perceived long-lasting benefits, and post-intervention mindfulness scores. This study suggests that the capacity to up-regulate hippocampus-somatomotor coactivation may index part of the individual benefit derived from mindfulness, supporting its role as a tool for emotion regulation and stress management.

neuroscience↗

bioRxiv2017

New insights on the pharmacogenomics of antidepressant response from the GENDEP and STAR*D studies: rare variant analysis and high-density imputation

Genome-wide association studies have generally failed to identify polymorphisms associated with antidepressant response. Possible reasons include limited coverage of genetic variants that this study tried to address by exome genotyping and dense imputation.\n\nA meta-analysis of Genome-Based Therapeutic Drugs for Depression (GENDEP) and Sequenced Treatment Alternatives to Relieve Depression (STAR*D) studies was performed at SNP, gene and pathway level. Coverage of genetic variants was increased compared to previous studies by adding exome genotypes to previously available genome-wide data and using the Haplotype Reference Consortium panel for imputation. Standard quality control was applied. Phenotypes were symptom improvement and remission after 12 weeks of antidepressant treatment. NEWMEDS consortium samples and Pharmacogenomic Research Network Antidepressant Medication Pharmacogenomic Study (PGRN-AMPS) served for replication.\n\n7,062,950 SNPs were analysed in GENDEP (n=738) and STAR*D (n=1409). rs116692768 (p=1.80e-08, ITGA9 (integrin alpha 9)) and rs76191705 (p=2.59e-08, NRXN3 (neurexin 3)) were significantly associated with symptom improvement during citalopram/escitalopram treatment. At gene level, no consistent effect was found. At pathway level, the Gene Ontology terms GO:0005694 (chromosome) and GO:0044427 (chromosomal part) were associated with improvement (corrected p=0.007 and 0.045, respectively). The association between rs116692768 and symptom improvement was replicated in PGRN-AMPS (p=0.047), while rs76191705 was not. The two SNPs did not replicate in NEWMEDS.\n\nITGA9 codes for a membrane receptor for neurotrophins and NRXN3 is a transmembrane neuronal adhesion receptor involved in synaptic differentiation. Despite their meaningful biological rationale for being involved in antidepressant effect, no convincing replication was achieved. Further studies may help in clarifying their role.

genomics↗