Almost one-third of all malignant melanoma patients exhibit emotional stress indicating the need for professional care. Considering this, patients’ psychological needs are routinely overlooked and unfulfilled, even though there is substantial evidence that psychological therapies may enhance psychosocial outcomes for melanoma patients, such as low mood, sadness, and anxiety. Among developing countries and some health systems in developed regions, the lack of awareness and screening methods for skin cancer creates a high risk of psychological issues associated with more advanced diseases. Therefore, the current study aimed to investigate and compare the impact of malignant melanoma awareness for screening, prevention, and treatment on the patient’s quality of life and coping with stress and depression, based on patients’ age. This cross-sectional study recruited 238 patients with malignant melanoma distributed into two groups, Group A patients between 18 and 65 years and Group B patients older than 65. There were no significant gender differences and cancer staging differences between groups, although self-reported depressed mood and anhedonia were significantly more frequent in younger adults with malignant melanoma (43.8% vs. 28.9%). From the unstandardized surveys, it was observed that significantly fewer patients from Group B knew that melanoma could be caused by sun exposure (34.2% vs. 52.2%), and they were less likely to use sunscreen or visit a doctor to evaluate their skin moles (25.9% vs. 14.5%). Elderly patients preferred television as the main source of information, and only 68.4% of patients from Group B were using smart devices. There was a significantly higher physical score on the SF-12 scale among Group A patients, although patients from Group B scored higher in the mental health assessment, and the perceived helplessness on the PSS-10 scale was significantly higher compared to younger adults with melanoma (2.97 vs. 2.71, p-value = 0.036). Lower scores on the physical and mental SF-12 questionnaire determined a higher presence of depressive symptoms (rho = −0.352, respectively rho = −0.273). Higher scores on the DLQI sexual difficulties and treatment difficulties also correlated significantly with the presence of depressive symptoms and anhedonia (rho = 0.341, respectively rho = 0.264). Awareness campaigns for malignant melanoma should focus on the elderly population, too, using the television as the main communication channel. On the other hand, the more informed and knowledgeable group of adults younger than 65 are more likely to experience psychological problems and should be targeted for psycho-oncological aid.

Background: Biomarkers play an important role in COVID-19, and more research in this regard is needed, especially in the case of children. This study aimed to look for a link between the C reactive protein (CRP), lactate dehydrogenase (LDH), creatine kinase (CK), vitamin D and COVID-19 in pediatric patients. Methods: This is a retrospective cohort study, performed on children diagnosed positively with COVID-19 at a children’s hospital in western Romania. Available CRP, LDH, CK vitamin D and clinical severity were recorded. For each biomarker, groups were formed by patients’ age. Mean/median group differences were assessed using Student’s t test or Mann–Whitney and Kruskal–Wallis with Dunn’s post hoc tests. Association was assessed using the chi² test, while correlation was assessed using Spearman’s rank correlation. Results: 181 positive children were studied between 1 August 2021 and 1 February 2022. Average age was 8.76 years (SD = 3.93). There were 94 (51.93%) males and 87 (48.07%) females. The cases were: 62 asymptomatic (34.25%), 107 mild (59.12%), 9 moderate (4.97%), 3 severe (1.66%). Regarding CRP, a significant difference between older and younger patients was observed (p = 0.0034). Clinical severity was associated with CRP (p = 0.0281), LDH (p = 0.0410) and vitamin D (p = 0.0444). Regarding CK, no differences or associations proved significant. Correlation testing was conducted for CRP, LDH, vitamin D and clinical signs. With the exception of LDH-CRP and LDH-vitamin D, all relationships proved statistically significant. Conclusions: CRP, LDH and vitamin D levels are important biomarkers for COVID-19-positive pediatric patients, while CK was mostly within normal ranges.

Alzheimer’s disease (AD) is the most prevalent cause of dementia, characterized by progressive cognitive decline, amyloid-β (Aβ) plaques, and neurofibrillary tangles composed of hyperphosphorylated tau protein. Other tauopathies, including frontotemporal lobar degeneration (FTLD), progressive supranuclear palsy (PSP), and corticobasal degeneration (CBD) share pathological hallmarks centered on abnormal tau biology. Increasing evidence highlights the role of post-translational modifications in modulating these pathogenic processes. Among these, glycosylation, the enzymatic attachment of glycans to proteins or lipids, has emerged as a critical regulator of protein folding, trafficking, aggregation, and clearance. Both N-linked glycosylation (N-glycosylation) and O-linked glycosylation (O-glycosylation) influence tau stability, Aβ processing, receptor signaling, synaptic integrity, and neuroinflammation. Dysregulated glycosylation patterns have been documented in brains and cerebrospinal fluid (CSF) of AD patients, suggesting biomarker potential and novel therapeutic targets. Moreover, glycosyltransferases and glycosidases show altered expression in neurodegeneration, linking metabolic and inflammatory pathways to tauopathy progression. This review synthesizes current evidence on the implications and consequences of glycosylation in AD and other tauopathies, integrating mechanistic, pathological, and clinical findings. We also discuss advances in glycoproteomics, the interplay between glycosylation and phosphorylation, and the translational potential of targeting glycosylation pathways for diagnosis and therapy.

Background/Objectives: Post-stroke cognitive impairment (PSCI) affects ~40% of survivors. Diffusion Tensor Imaging Analysis Along the Perivascular Space (DTI-ALPS) is a fast, contrast-free surrogate of perivascular (glymphatic-aligned) diffusivity that may stratify PSCI risk. We systematically synthesized evidence on the diagnostic and prognostic performance of ALPS in ischemic stroke. Methods: Following PRISMA 2020, we searched PubMed/MEDLINE, Scopus, and Web of Science from inception to August 2025 for human ischemic stroke studies reporting ALPS and cognitive or functional outcomes. Eligible designs were cohort or case–control. Outcomes included group differences, associations with cognition (Montreal Cognitive Assessment [MoCA]/Mini-Mental State Examination [MMSE]), prognostic accuracy for PSCI/functional outcome, and longitudinal change. Risk of bias was appraised with QUADAS-2 (diagnostic) and QUIPS (prognostic). The protocol was registered on OSF. Heterogeneity among studies precluded a meta-analysis. Results: Five single-center cohorts (n per cohort 29–120) from Asia, Europe, and the USA used 3T DTI with ventricular-level ALPS ROIs. Across studies, ALPS was lower after stroke, with early ipsilesional depression and partial recovery over weeks to months. ALPS correlated with cognition (MoCA r ≈ 0.43–0.56) and discriminated early cognitive impairment (AUC 0.868; sensitivity 96%, specificity 66%). Follow-up ALPS predicted poor 6-month outcome (AUC 0.786). In lacunar stroke with small-vessel disease, higher baseline ALPS related to better cognitive trajectories and lower incident dementia risk (HR ≈ 0.33), though associations attenuated after adjustment for diffusion microstructural covariates (PSMD/MD). Reporting of acquisition parameters and ROI methods varied; overall risk of bias was moderate. Conclusions: DTI-ALPS shows consistent post-stroke reductions, recovery-sensitive trajectories, and promising—though context-dependent—prognostic value for PSCI and longer-term outcomes. Clinical translation will require standardized acquisition/analysis, multimodal adjustment, prespecified cut-offs, and prospective multicenter validation.

Background and Objectives: Optic disc drusen (ODD) can mimic papilledema and are linked to structural crowding, microvascular change, and visual-field loss. We synthesized structural/microvascular differences, functional status and change, diagnostic performance, and ODD–NAION co-occurrence. Methods: This study used PRISMA-aligned searches of PubMed, Embase, and Web of Science (inception–15 July 2025). Eligible designs included cross-sectional, cohort, and diagnostic accuracy studies with numeric outcomes (OCT/OCTA, visual fields, test accuracy, NAION prevalence). Two reviewers independently screened, extracted, and appraised bias. Heterogeneity precluded meta-analysis; narrative synthesis was used. Bias risk was moderate. Results: From 359 records, 6 studies met the criteria. ODD eyes showed thicker RNFL than controls (117.54 ± 18.75 vs. 105.81 ± 14.45 µm; 101 ± 12 vs. 97 ± 10 µm) and worse baseline mean deviation (−1.78 ± 3.87 dB). OCTA demonstrated sectoral peripapillary vessel-area density reduction (inferior 0.30 vs. 0.34; temporal 0.44 vs. 0.48; superonasal 0.44 vs. 0.49). Visual-field phenotypes were normal (44–52%), enlarged blind spot (19–29%), and other localized defects (24–29%); the longitudinal decline averaged −0.23 ± 0.26 dB/year with 88% slow progressors. In pseudopapilledema, single-test yields were ultrasound at 87.2%, OCT at 80.2%, and FAF at 62.8%; OCT alone distinguished buried ODD from mild papilledema with 50–64% accuracy (κ ≈ 0.35). Among young NAION, ODD affected 56.7% of patients and 53.3% of eyes; bilaterality was 95.2%, and only 35.9% were ophthalmoscopically visible. Conclusions: Multimodal imaging shows structural thickening, microvascular rarefaction, and modest functional loss in ODD, with slow average progression. In suspected papilledema, protocolized multimodal workflows outperform OCT alone. ODD are common in young NAION, supporting risk stratification and longitudinal monitoring.

Alzheimer’s disease (AD) is the most prevalent cause of dementia, characterized by progressive cognitive decline, amyloid-β (Aβ) plaques, and neurofibrillary tangles composed of hyperphosphorylated tau protein. Other tauopathies, including fronto-temporal lobar degeneration (FTLD), progressive supranuclear palsy (PSP), and corti-cobasal degeneration (CBD), share pathological hallmarks centered on abnormal tau biology. Increasing evidence highlights the role of post-translational modifications in modulating these pathogenic processes. Among these, glycosylation, the enzymatic attachment of glycans to proteins or lipids, has emerged as a critical regulator of pro-tein folding, trafficking, aggregation, and clearance. Both N-linked glycosylation (N-glycosylation) and O-linked glycosylation (O-glycosylation) influence tau stabil-ity, Aβ processing, receptor signaling, synaptic integrity, and neuroinflammation. Dysregulated glycosylation patterns have been documented in brains and cerebrospi-nal fluid (CSF) of AD patients, suggesting biomarker potential and novel therapeutic targets. Moreover, glycosyltransferases and glycosidases show altered expression in neurodegeneration, linking metabolic and inflammatory pathways to tauopathy pro-gression. This review synthesizes current evidence on the implications and conse-quences of glycosylation in AD and other tauopathies, integrating mechanistic, pathological, and clinical findings. We also discuss advances in glycoproteomics, the interplay between glycosylation and phosphorylation, and the translational potential of targeting glycosylation pathways for diagnosis and therapy.