Cognitive dysfunction represents one of the most persistent and disabling features of Long COVID, yet its molecular underpinnings remain incompletely understood. This narrative review synthesizes current evidence on the pathophysiological mechanisms linking SARS-CoV-2 infection to long-term neurocognitive sequelae. Key processes include persistent neuroinflammation, blood–brain barrier (BBB) disruption, endothelial dysfunction, immune dysregulation, and neuroendocrine imbalance. Microglial activation and cytokine release (e.g., IL-6, TNF-α) promote synaptic dysfunction and neuronal injury, while activation of inflammasomes such as NLRP3 amplifies CNS inflammation. Vascular abnormalities, including microthrombosis and BBB leakage, facilitate the infiltration of peripheral immune cells and neurotoxic mediators. Hypothalamic–pituitary–adrenal axis dysfunction and reduced vagal tone further exacerbate systemic inflammation and autonomic imbalance. Biomarkers such as GFAP, NFL, IL-6, and S100B have been associated with both neuroinflammation and cognitive symptoms. Notably, transcriptomic signatures in Long COVID overlap with those observed in Alzheimer’s disease, highlighting shared pathways involving tau dysregulation, oxidative stress, and glial reactivity. Understanding these mechanisms is critical for identifying at-risk individuals and developing targeted therapeutic strategies. This review underscores the need for longitudinal research and integrative biomarker analysis to elucidate the molecular trajectory of cognitive impairment in Long COVID.

Background: Palliative care has emerged as a key component in the management of chronic heart failure, addressing persistent physical and psychosocial symptoms that often remain insufficiently controlled by conventional cardiology. This systematic review aimed to evaluate the impact of palliative care interventions on symptom burden, quality of life (QoL) and decision-making processes in adults with chronic heart failure. Methods: A systematic search of PubMed, Scopus and Web of Science identified studies published between January 2005 and February 2025. Eligible designs included randomized controlled trials, observational cohorts and qualitative studies. The review followed PRISMA 2020 guidelines. Methodological quality was assessed using the Cochrane Risk of Bias 2.0 (RoB 2.0), Risk of Bias in Non-Randomized Studies of Interventions (ROBINS-I) and Joanna Briggs Institute (JBI) appraisal tools. Due to heterogeneity in study designs and outcomes, a narrative synthesis was conducted. Results: Nineteen studies met the inclusion criteria. Palliative care interventions consistently reduced dyspnea, fatigue, anxiety and depression and were associated with improved functional status and QoL. Integrated palliative–cardiology programs were linked to fewer hospital readmissions, shorter hospital stays and increased documentation of advance care planning. However, methodological variability, small sample sizes and non-standardized outcome measures limited comparability across studies. Conclusions: The evidence supports the early incorporation of palliative care into routine management of chronic heart failure. Early, multidisciplinary and patient-centered approaches enhance clinical and psychosocial outcomes while improving healthcare efficiency and ensuring that care aligns with patients’ goals, values and quality-of-life priorities.

Post-viral neuroinflammatory syndromes, particularly those occurring after SARS-CoV-2 infection, have received increasing attention due to their complex and persistent neurological manifestations. The aim of this narrative review is to integrate current evidence on the molecular and cellular mechanisms underlying chronic neuroinflammation following viral infections, with a focus on dysregulated innate immune responses, macrophage–microglia interactions, oxidative–mitochondrial stress, and impaired inflammation resolution pathways. Our synthesis shows that prolonged activation of macrophages and glial cells promotes the continuous release of pro-inflammatory mediators, while defective phagocytosis and inadequate clearance of cellular debris maintain an inflammatory microenvironment. Mitochondrial dysfunction further amplifies immune activation by stimulating metabolic stress and reactive oxygen species production. In parallel, deficiencies in mediators specialized in inflammation resolution impede the transition from inflammation to resolution, allowing neuroimmune imbalance and nociceptive sensitization to persist long after virus clearance. Key conclusions indicate that these interconnected mechanisms collectively contribute to the long-term neurological symptoms observed in post-viral states, including cognitive impairment, neuropathic pain, and fatigue. Emerging therapeutic strategies targeting cytokine signaling, microglial reactivity, mitochondrial function, and resolution pathways are promising, but remain insufficiently validated in clinical practice. Overall, evidence suggests that post-viral neuroinflammation results from the convergence of sustained immune activation and failure of endogenous resolution mechanisms, highlighting the need for further mechanistic studies and targeted interventions.

In Romania, as in other parts of the world, the family doctor is the first to make contact with a healthy patient and is also the first to notice even the smallest pathological changes. In the context of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, the patient's communication with the family doctor became even closer and some behavioral changes could be easily noticed. To assess the symptoms of anxiety and depression in the Romanian population using social media platforms in the context of the COVID-19 pandemic. We conducted an anonymous, web-based cross-sectional survey consisting of 31 questions related to general characteristics (age, gender, education, inhabitancy, residence, smoking status, and alcohol consumption) and adapted GAD-7 (7-item General Anxiety Disorders questionnaire) and PHQ-9 (9-item Patient Health Questionnaire). This questionnaire was sent to volunteers in an electronic format through a social network (Facebook, Twitter). The data collected were statistically processed using IBM SPSS v25.0 (IBM Corp., Armonk, NY). The inclusion criteria were age over 18 years and no history of chronic disease. The exclusion criteria consisted of the absence of a mental illness diagnosis. From the 1254 respondents, 1232 cases were selected for statistical analysis after applying the exclusion criteria. The mean age was 35.94 (SD = 11.4, 95%CI=10.9-11.9) with a minimum of 18 years and a maximum of 97 years. Eighty-four point nine percent (84.9%; N=1046) of all study participants are female and 79.13% (N= 975) live in the urban area. A total of 188 (15.25%) were diagnosed with COVID-19 of which 31 (16.66%) were male and 157 (15%) were female. N=170 (13.8%) reported moderate symptoms of anxiety during the last two weeks before the survey while N=96 (7.8%) had severe anxiety. Twenty-two point two percent (22.2%; N=274) of the participants reported moderate symptoms of depression while 10.1% (N=125) had moderately severe symptoms and 6.6% (N=81) could be diagnosed with severe depression. A greater likelihood of screening for depression diagnosis was associated with ages between 25 and 34 years (OR=0.90, 95%CI=0.86-0.94, P<.001), 35 and 44 years (OR=0.88, 95%CI=0.84-0.93, P<.001), and 45 and 54 years (OR=0.87, 95%CI=0.82-0.92, P<.001). Also, a tendency was observed for women to be more prone to high levels of anxiety (OR=1.21, 95%CI=1.08-1.35, P< .001) and depression (OR=2.16, 95%CI=1.51-308, P< .005). Regarding the high prevalence of depression and anxiety, especially in women, appropriate measures for the risk categories should be applied. In the new social context created by the COVID-19 pandemic, screening for psychiatric and psychological disorders should be performed by telemedicine.

Classic polyarteritis nodosa (PAN) is a vasculitis with systemic manifestations that is characterized by inflammatory and necrotizing lesions affecting medium and small muscular arteries, most frequently at the bifurcation of the vessels. These lesions lead to the formation of microaneurysms, hemorrhaging ruptured aneurysms, thrombosis, and, consequently, ischemia or organ infarction. Background and Objectives: We present a complex clinical case of a patient with a late diagnosis of polyarteritis nodosa with multiorgan involvement. Materials and Methods: The 44-year-old patient, in an urban environment, presented on her own in the emergency room for acute ischemia phenomena and forearm and right-hand compartment syndrome, requiring surgical decompression in the Plastic Surgery Clinic. Results: Significant inflammatory syndrome is noted, alongside severe normocytic hypochromic iron deficiency anemia, nitrogen retention syndrome, hyperkalemia, hepatic syndrome, and immunological disturbances: absence of cANCA, pANCA, anti Scl 70 Ac, antinuclear Ac, and anti dDNA Ac, as well as a low C3 fraction of the plasmatic complement system. The morphological aspect described in the right-hand skin biopsy correlated with the clinical data supports the diagnosis of PAN. Conclusions: The viral form of PAN seems to be individualized as a distinct entity, requiring early, aggressive medication.

Background/Objectives: Advanced heart failure (HF) carries a high symptom burden and mortality, and identifying the right time for palliative and advanced-therapy discussions remains difficult. We systematically reviewed the prognostic value of serological biomarkers, echocardiographic indices, and patient-reported outcomes (PROs) in advanced HF. Methods: PubMed, Scopus, Web of Science, and the Cochrane Library were searched on 1 June 2026 for studies published within the prior 10 years, following PRISMA 2020 (PROSPERO CRD420261505929). Risk of bias was assessed with the Newcastle–Ottawa Scale and certainty of evidence with GRADE. Hazard ratios (HRs) for all-cause mortality were pooled with random-effects models within pathophysiologically defined serological subgroups; markers with opposing prognostic directions were synthesized narratively. Results: Of 3866 records, 37 studies (approximately 31,849 patients) were included; 29 (78%) were at low risk of bias. The pooled HR was 1.35 (95% CI 1.06–1.74; k = 4; I² = 92%) for neurohormonal/congestive markers; exploratory two-study estimates were 1.75 (1.50–2.04; I² = 6%) for renal/cardiorenal and 2.17 (0.85–5.52; I² = 86%) for inflammatory-nutritional markers. GRADE certainty was Low for the renal/cardiorenal estimate and Very Low for the other two, and funnel-plot asymmetry suggested small-study effects. Echocardiographic and PRO markers were individually associated with prognosis but showed opposing directions within outcome categories and were not pooled. Conclusions: Serological, echocardiographic, and patient-reported markers each carry prognostic information in advanced HF, but the pooled estimates are exploratory. Most studies assessed mortality or hospitalization rather than palliative or advanced-therapy decisions; relevance to such decisions is interpretive and requires prospective confirmation.