Alzheimer's disease (AD) is a progressive neurodegenerative disorder and a growing public health concern. Its core pathological features include cerebral amyloid-β deposition and tau aggregation. mRNA translation is a tightly regulated process essential for gene expression and protein synthesis. It plays critical roles in neural development, synaptogenesis, and synaptic plasticity. In recent years, dysregulated translational control has been recognized as an important pathogenic mechanism in several neurological diseases, including AD. This review provides an integrated overview of the biological basis and mechanisms of dysregulated mRNA translation in AD, including translation initiation and elongation, local synaptic translation, abnormalities in RNA-binding proteins and stress granules, tRNA dysregulation, and the effects of AD-related genetic factors on translational control. Beyond the classic mechanisms of protein aggregation, the onset and progression of AD are also accompanied by abnormal translational regulation, involving initiation, elongation, and local synaptic translation. A major feature of these abnormalities is the coexistence of suppressed global protein synthesis and selectively enhanced translation of certain disease-related mRNAs, involving the integrated stress response, eIF2α/eIF4E signaling, eEF2K/eEF2 pathway, and RNA-binding protein dysfunction. Translational dysregulation provides a new perspective for understanding the molecular pathology of AD and has prompted the exploration of interventions targeting key nodes in translational control. Strategies targeting the integrated stress response, cap-dependent translation initiation, eEF2K, and tau-RNA-binding protein interactions have shown potential to improve synaptic function and cognitive phenotypes in animal models, although their safety and clinical translatability require further evaluation. This review provides an up-to-date reference for understanding translation-centered mechanisms in AD and evaluating emerging therapeutic strategies targeting translational control.

Sarcopenia is a prevalent geriatric syndrome, and nutritional intervention plays an important role in its prevention and management. In recent years, anti-inflammatory dietary strategies have received increasing attention in clinical guidelines; however, their awareness, implementation, and support needs in real-world care settings remain insufficiently explored. This study aimed to investigate the lived experiences and practical challenges of anti-inflammatory dietary management in sarcopenia care from a multi-stakeholder perspective, providing evidence for the development of continuous nutritional management strategies.

Alzheimer's disease (AD) is the leading cause of dementia worldwide, disproportionately affecting individuals over 65 years of age and imposing a rapidly escalating burden on healthcare systems and caregivers globally. For decades, management relied on symptomatic agents-cholinesterase inhibitors and memantine-that provide modest cognitive benefits without altering disease progression. The recent approvals of the anti-amyloid monoclonal antibodies lecanemab (2023) and donanemab (2024) represent a paradigm shift, offering the first therapies that modestly but significantly slow clinical decline by targeting the underlying amyloid-β pathology. However, these advances are accompanied by important safety concerns, particularly amyloid-related imaging abnormalities, substantial costs, and unresolved questions regarding long-term clinical meaningfulness and equitable access. This comprehensive review synthesizes current knowledge across the full spectrum of AD, encompassing molecular pathophysiology (amyloid cascade, tau hyperphosphorylation, and neuroinflammation), genetic architecture (familial mutations and APOE-mediated risk), evolving biomarker-based diagnostic frameworks, established symptomatic treatments, and newly approved disease-modifying agents. We further examine emerging therapeutic strategies, including tau-targeted therapies, neuroinflammation-directed approaches, multi-target and combination strategies, drug delivery innovations, and prevention trials in preclinical populations. Throughout, we critically evaluate the evidence, acknowledging controversies and limitations while identifying promising future directions. Importantly, integrating these diagnostic and genetic advances into geriatric care settings presents unique implementation challenges, as aging populations often face comorbidities, polypharmacy, and limited access to specialized diagnostic infrastructure. As AD therapeutics enter a new era, integrating pharmacological interventions with biomarker-guided patient selection, rigorous safety monitoring, and modifiable risk factor management will be essential for optimizing outcomes in aging populations.

The global aging population faces an increasing burden of chronic multimorbidity, much of which is driven by inflammaging. Inflammaging is defined as a persistent, low-grade inflammatory state recognized as a hallmark of biological aging. This narrative review examines therapeutic strategies targeting key mechanisms of inflammaging, with particular focus on cellular senescence and the senescence-associated secretory phenotype (SASP), nicotinamide adenine dinucleotide (NAD+) decline, and inflammasome activation. Senolytic therapies designed to eliminate senescent cells have progressed into early-phase clinical trials. Combinations such as dasatinib plus quercetin and the flavonoid fisetin have reduced circulating SASP factors in early studies. Senomorphic agents, including rapamycin and Janus kinase (JAK) inhibitors, represent an alternative strategy by suppressing SASP production while preserving cell viability. Another therapeutic approach focuses on restoring intracellular NAD[+] levels. Supplementation with precursors such as nicotinamide riboside and nicotinamide mononucleotide has shown beneficial effects on vascular function and metabolic health in early human studies. In addition, inhibition of the NAD[+]-consuming enzyme CD38 represents a complementary strategy aimed at preserving NAD[+] availability. Targeted anti-inflammatory biologics directed against cytokines such as IL-1β, IL-6, and TNF-α have demonstrated clinical benefits in cardiovascular disease, supporting inflammation-targeted therapy. Repurposed metabolic medications including metformin, sodium-glucose cotransporter-2 inhibitors, and glucagon-like peptide-1 receptor agonists also exhibit anti-inflammatory effects. In addition, evidence-based lifestyle interventions including caloric restriction, regular exercise, and Mediterranean dietary patterns remain important complementary strategies for mitigating inflammaging. Despite progress, translating these findings into clinical practice remains challenging because validated biomarkers are limited, trial designs are complex, and long-term safety data are still needed. Future collaborative research will help evaluate combination strategies and precision approaches targeting biological aging mechanisms.