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.

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.

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.

Background and Objectives: Different types of food introduced gradually in the diet will expose children to different food allergens, increasing the chance of developing allergic diseases. The aim of our study was to determine if allergen-specific IgE values can influence, depending on the diet, the prediction of remission of urticaria in children. Materials and Methods: This prospective study was conducted in 132 patients diagnosed over two years with urticaria, admitted to “Sf. Maria” Clinical Pediatric Hospital Iaşi. Total IgE assay was performed by ELISA, and determination of specific serum IgE by the CLA System Quanti Scan method (Innogenetics, Heiden, Germany). Data were gathered and statistical analysis was performed using statistical software SPSS, using descriptive and inferential statistics. Results: The determination of specific IgE to food allergens was performed on a total of 132 cases. The values of specific IgE were positive for one or more food allergens in 84 patients (63.64%). The most common allergens involved were: cow’s milk in 33.3% cases, egg white in 22.6% cases, and hazelnuts in 11.9% cases. The specific IgE values for the different types of food included in our study had a predictive value for disease remission. Conclusions: The determination of specific IgE confirms the presence of a particular food allergen and may have predictive value for the future development of an allergic manifestation.

Glucagon-like peptide-1 receptor agonism has attracted interest in neurodegeneration because of its effects on metabolic and inflammatory pathways implicated in neuronal dysfunction. This narrative review examines the molecular rationale and neurological evidence for selective glucagon-like peptide-1 receptor agonists, dual agonists additionally targeting the glucose-dependent insulinotropic polypeptide receptor, and triple agonists also engaging the glucagon receptor. English-language literature retrieved from PubMed, Scopus, and Web of Science was synthesized according to study design and neurological relevance. Preclinical findings indicate modulation of insulin signaling, synaptic function, mitochondrial homeostasis, and neuroinflammation, but responses vary across compounds and experimental models. In Alzheimer’s disease, liraglutide did not meet its primary trial endpoint, and semaglutide did not slow clinical progression. Parkinson’s disease trials have yielded mixed results without establishing disease modification. Observational associations with reduced dementia risk remain susceptible to confounding. Neurological evidence for tirzepatide and retatrutide remains predominantly observational or preclinical. Greater metabolic efficacy does not establish neuroprotection, while nutritional vulnerability may constrain therapeutic applicability. Dedicated randomized trials integrating clinical outcomes with pharmacological exposure, target engagement, and metabolic mediation are required to distinguish systemic effects from direct neural actions and determine whether these therapies can prevent cognitive decline or modify established neurodegenerative disease.

Background/Objectives: The Mini-Mental State Examination (MMSE), Clock Drawing Test (CDT), and Reisberg Global Deterioration Scale (GDS) are used together in primary care. This study describes their score distributions across operational severity strata in a Romanian cohort. Methods: We conducted a cross-sectional descriptive study of a selected cohort of 326 adults aged ≥50 years with suspected cognitive impairment in three family medicine practices in Iași. One unblinded clinician administered all instruments and assigned the strata by integrated clinical assessment of functional status, MMSE performance, and Reisberg GDS staging, with approximate reference bands for both scales. Scores and their positions relative to these bands were summarised descriptively. Results: The strata comprised 53 participants with mild, 247 with moderate, and 26 with severe cognitive impairment; 39.3% of participants were illiterate or had ≤4 years of schooling. Cohort medians (ranges) were 15 (0–25) for the MMSE, 4 (0–10) for the CDT, and 5 (1–7) for the Reisberg GDS. In the mild and moderate strata, respectively, 30.2% and 30.0% of MMSE scores and 26.4% and 27.5% of Reisberg stages lay outside the approximate reference bands. Conclusions: Because MMSE and Reisberg information contributed to the classification, the assessor was not blinded, and the severe stratum was small, these descriptive results cannot establish diagnostic discrimination or comparative measurement performance.