Introduction: Post-COVID-19 Condition (PCC), commonly referred to as long COVID, has become a major post-pandemic health issue, with many individuals experiencing persistent cognitive and neuropsychiatric symptoms. These difficulties, often described as “brain fog”, include problems with memory, executive functioning and processing speed, and can markedly disrupt daily life, emotional well-being and work capacity. Methods: A narrative review was performed using PubMed and Google Scholar. Keywords included “post-COVID cognitive impairment”, “long COVID”, “neurocognitive dysfunction”, and related terms. Original studies, cohort research, systematic reviews and meta-analyses were screened for relevance. Documents from WHO, NICE were also reviewed to supplement diagnostic definitions. Results: Current studies consistently indicate that cognitive impairment represents one of the most common manifestations of long COVID, with estimates ranging from 20% to 30%. Difficulties with executive function, memory, sustained attention and information-processing speed form the core pattern of impairment and exert a meaningful impact on daily independence and well-being. Neuroimaging findings support these complaints, showing corresponding metabolic, structural and microvascular changes. Proposed mechanisms most often involve sustained neuroinflammation, immune imbalance, endothelial injury and microvascular dysfunction. Conclusions: Post-COVID cognitive impairment remains a significant clinical challenge, affecting daily functioning and long-term recovery for many patients. Clearer diagnostic criteria and improved assessment tools integrating neuropsychological testing, imaging and biomarker data are needed to enhance recognition and to identify those at higher risk. Ongoing research into therapeutic strategies remains essential for optimising long-term management and outcomes in affected patients.

Age-related macular degeneration (AMD) remains the leading cause of irreversible central vision loss in the elderly. Increasing attention has been directed toward lipid metabolism as a potential contributor to disease onset and progression. The overlap between AMD and atherosclerosis—particularly regarding lipid accumulation, endothelial dysfunction, and chronic inflammation—has prompted interest in lipid-lowering therapies. This narrative review synthesizes the clinical evidence published between 2020 and 2025 on the potential role of statins and fenofibrate in AMD risk modification and disease progression. A structured literature search was conducted in PubMed, Scopus, and Web of Science using combined MeSH and free-text terms related to lipid-lowering agents and AMD. Human studies evaluating clinical incidence or progression outcomes were considered alongside contextual evidence from prior evidence syntheses. Overall, findings remain heterogeneous. Most studies did not demonstrate a consistent association between statin therapy and AMD incidence or progression in unselected populations. However, selected reports suggested a potential delay in dry AMD onset or slower disease progression among patients receiving prolonged or higher-intensity statin treatment. Evidence regarding fenofibrate was more limited and heterogeneous, with only a tentative protective signal observed in adherent users, particularly for non-exudative AMD. The current literature does not support lipid-lowering therapy as a universal preventive strategy for AMD. Nonetheless, subgroup-specific benefits cannot be excluded, especially in early disease stages or metabolically high-risk populations. Further well-designed prospective and randomized studies are needed to clarify therapeutic relevance and identify the patients who are most likely to benefit.