Synaptic vesicle proteins 2 (SV2) were discovered in the early eighties, but the clear demonstration that SV2A is the target of efficacious anti-epileptic drugs from the racetam family stimulated efforts to improve understanding of its role in the brain. Many functions have been suggested for SV2 proteins including ions or neurotransmitters transport or priming of synaptic vesicles. Moreover, several recent studies highlighted the link between SV2 and different neuronal disorders such as epilepsy, schizophrenia, Alzheimer’s or Parkinson’s disease. In this review, we will summarize our present knowledge on SV2A function(s) and its potential role(s) in the pathophysiology of various brain disorders.

Parvalbumin-positive neurons are inhibitory neurons that release GABA and are mostly represented by fast-spiking basket or chandelier cells. They constitute a minor neuronal population, yet their peculiar profiles allow them to react quickly to any event in the brain under normal or pathological conditions. In this review, we will summarize the current knowledge about the fundamentals of fast-spiking parvalbumin-positive neurons, focusing on their morphology and specific channel/protein content. Next, we will explore their development, maturation, and migration in the brain. Finally, we will unravel their potential contribution to the physiopathology of epilepsy.

Breast cancer is the leading cause of cancer death in women worldwide. Trastuzumab, the main HER2-targeted treatment, faces limitations due to potential cardiotoxicity. The management of patients with mild cardiotoxicity on trastuzumab remains uncertain, resulting in treatment discontinuation and negative oncological outcomes. This retrospective study analyzed 23 patients who experienced decreased left ventricular function during trastuzumab treatment. During the 18-month follow-up period, two patients (9%) had severe declines in function, leading to treatment cessation, and one patient (4%) developed heart failure symptoms. However, 21 patients showed mild, reversible myocardial dysfunction without significant differences in final ventricular function compared to a control group (58.4% vs. 61.7%, respectively; p = 0.059). The declines in function were most pronounced at nine months but improved at twelve and eighteen months. Various echocardiographic parameters changed significantly over time. As predictors of severe cardiotoxicity, we identified the following: LVEF before initial chemotherapy (p = 0.022), as well as baseline LVEF before treatment with trastuzumab (p = 0.007); initial left ventricular end systolic volume (p = 0.027); and the initial global longitudinal strain (p = 0.021) and initial velocity time integral in the left ventricular outflow track (p = 0.027). In conclusion, the continuation of trastuzumab should be considered for most patients with mild cardiotoxicity, with close cardiac monitoring and cardioprotective measures. However, identifying the patients at risk of developing severe cardiotoxicity is necessary. According to our data, the initial LVEF and GLS levels appear to be reliable predictors.

Background: Many studies recognize a close link between inflammation, cardiovascular disease (CVD), and oncological diseases. High-sensitivity C-reactive protein (hs-CRP), a marker of low-grade systemic inflammation, is a shared feature of these conditions. This retrospective study aims to assess the predictive value of hs-CRP for the development of cancer in patients with CVD. Methods: Analyzing data from 174 patients undergoing coronary angiography, we assessed hs-CRP levels and collected demographic, biological, and therapeutic data that could influence the studied parameters. Results: Only smoking and dyslipidemia correlated significantly with CRP levels (p = 0.018 and 0.049, respectively). However, hs-CRP did not predict cancer development (p = 0.52) but correlated with 1-year and follow-up mortality (p = 0.011 and 0.021, respectively). Antiplatelet and statin use was higher in the cancer-free group and associated with a lower probability of developing cancer (p < 0.001 and p = 0.009, respectively). Conclusions: While hs-CRP did not prove effective as a cancer predictor in our study, it correlated with all-cause mortality. Our findings suggest a potential protective effect of antiplatelet and statin treatments against cancer development, prompting further research to understand underlying processes and identify key factors in the pathophysiology of these diseases.

Myotoxicity, defined as immune-mediated injury to cardiac and/or skeletal muscle, has emerged as one of the most severe and lethal immune-related adverse events (irAE) in patients receiving immune checkpoint inhibitors (ICIs). Although myocarditis in oncology is not restricted to ICIs and may also occur after traditional cytotoxic chemotherapy, radiotherapy, or selected targeted therapies, ICI-associated cardiomyotoxicity is distinguished by its early onset, frequent overlap with myositis, and myasthenia gravis, and high case-fatality rate. This review outlines myotoxicity within the broader context of cancer therapy-related cardiovascular toxicity, then focuses on the distinct syndromes associated with different immunotherapy classes. For ICIs, we detail a spectrum including myocarditis, myositis, and overlap syndromes, quantified by data from large registries. For Chimeric Antigen Receptor (CAR) T-cell therapy, we focus on cardiotoxicity in the context of cytokine release syndrome (CRS). Diagnostic sections discuss clinical presentation, biomarkers, and imaging, emphasizing the need for troponin I over T and the nuanced interpretation of cardiac magnetic resonance (CMR). The POWER risk score is presented as the first externally validated tool to predict early major adverse cardiomyotoxic events (MACE) from ICIs. Finally, the review proposes distinct management strategies for ICI- versus CAR-T-related toxicity and outlines pragmatic surveillance protocols.