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                    <title><![CDATA[Current Aging Science (Volume 19 - Issue 2)]]></title>

                    <link>https://www.benthamscience.com/journal/103</link>

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                    RSS Feed for Journals <![CDATA[Current Aging Science]]> | BenthamScience

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                    <pubDate>2026-06-03</pubDate>

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                    <title><![CDATA[Current Aging Science (Volume 19 - Issue 2)]]></title>

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                    <link>https://www.benthamscience.com/journal/103</link>

                    </image><item><title><![CDATA[Demographic Shifts and Disease Burden in Brazil: Analyzing Future Healthcare Trends and Expenditure Needs]]></title><link>https://www.benthamscience.com/article/149787</link><pubDate>2026-06-03</pubDate><description><![CDATA[This perspective paper presents an in-depth analysis of the demographic shifts and changing disease burden in Brazil, exploring their profound impact on future healthcare trends and expenditure requirements. Brazil, with its vast and diverse population, is witnessing significant demographic transformations, including an aging populace and a notable shift in disease patterns. These changes are steering the country towards a heightened burden of chronic noncommunicable diseases, even as it continues to grapple with existing infectious diseases. Using data extracted from the Institute for Health Metrics and Evaluation database and published in the 2017 Global Disease Burden Study, the paper examines current demographic trends in Brazil, emphasizing the increasing proportion of the elderly and the consequent rise in age-associated health conditions, such as cardiovascular diseases, diabetes, and cancers. It highlights the implications of these shifts on the healthcare system, particularly the increased demand for long-term healthcare services and the challenge of providing comprehensive care within Brazil's existing healthcare infrastructure. This transition poses significant challenges in healthcare financing and resource allocation, necessitating strategic healthcare planning and substantial investments. This paper also explores potential strategies for addressing these emerging healthcare challenges. It advocates for the strengthening of primary healthcare services, investment in preventive healthcare measures, and the integration of advanced healthcare technologies. It provides projections for future healthcare expenditures in Brazil and highlights the need for efficient and targeted healthcare spending, aligned with the evolving demographic and disease profiles. Additionally, it underscores the importance of a multi-faceted approach involving government, private sector, and community collaboration for a robust and sustainable healthcare system.]]></description> </item><item><title><![CDATA[Deciphering the Potential of Bone Morphogenetic Pathway (BMP) in the Pathogenesis of Depression]]></title><link>https://www.benthamscience.com/article/149998</link><pubDate>2026-06-03</pubDate><description><![CDATA[Depression is a prevalent mental health disorder, profoundly impacting individuals and often exacerbated by stressful experiences. Current treatment options have limitations, including reduced efficacy and undesirable side effects. While antidepressant medications target distinct brain regions, their precise mechanisms influencing behavior remain incompletely elucidated. Recent research underscores the significance of the bone morphogenetic protein (BMP) signaling pathway within the hippocampus in mediating the effects of various antidepressants. Notably, these drugs inhibit BMP signaling, thereby augmenting neurogenesis in the hippocampus. Inhibiting BMP signaling specifically in newly generated brain cells elicits antidepressant effects, whereas suppressing these cells impedes such outcomes. This underscores the pivotal role of BMP signaling in the mechanism of antidepressant action. Adult neurogenesis, particularly in the hippocampus, emerges as pivotal for emotional regulation and stress response. Stress reduces the generation of new brain cells, whereas prolonged use of antidepressants promotes neurogenesis, suggesting a link between neurogenesis and depression. Investigating the molecular and cellular mechanisms underlying depression, anxiety, and antidepressant efficacy holds promise for the development of improved treatments characterized by rapid relief and reduced side effects.]]></description> </item><item><title><![CDATA[Allicin and its Therapeutic Potential in Diabetes Management: A Comprehensive Review]]></title><link>https://www.benthamscience.com/article/148998</link><pubDate>2026-06-03</pubDate><description><![CDATA[It has been known since ancient times that garlic (Allium sativum), a member of the Alliaceae family, is an indispensable component of human food. This compound contains abundant nutrients, minerals, sulphur-containing compounds, essential oils, phenols, and free amino acids. Sugar levels in the blood that are abnormally high are a symptom of diabetes mellitus, in which the body has difficulty appropriately regulating glucose metabolism. Elevated levels of glucose in blood plasma are considered DM. It has been suggested that two primary mechanisms are responsible for the pathogenesis of the disease. One of the main causes of the persistent hyperglycemia linked to diabetes mellitus is the immune system's devastation of pancreatic β-cells, which results in a lack of insulin synthesis. Additionally, endogenous resistance of the body cells to the action of insulin is also a contributing factor. Children who have type 1 diabetes frequently experience symptoms such as polyuria, weight loss, and polydipsia of varying degrees. A comprehensive literature search on the potential benefits of allicin in diabetes mellitus (DM) was conducted using reputable databases such as PubMed, Web of Science, Scopus, and other recognized scientific sources. Furthermore, information on the clinical application of allicin was reviewed and compiled from ClinicalTrials.gov to provide insights into ongoing and completed clinical studies. Allicin is a compound that has the potential to have effects on pancreatic cells, wound healing, promoting insulin secretion, diabetic macroangiopathy, maintaining glucose homeostasis, and diabetic nephropathy. In addition, studies on cell lines that were carried out with different concentrations of allicin demonstrated a significant inhibitory effect on diabetes mellitus. The promising treatment strategy, therapeutic benefits, and inhibitory actions that allicin exhibits on diabetes make it an appealing candidate for additional research and the possibility of its application in the treatment of diabetes mellitus.]]></description> </item><item><title><![CDATA[The Therapeutic Potential of Targeting the Pd-L1/Pd-1 Immune Checkpoint Pathway in Alzheimer's Disease]]></title><link>https://www.benthamscience.com/article/144768</link><pubDate>2026-06-03</pubDate><description><![CDATA[<p>Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by the accumulation of amyloid-β plaques, neurofibrillary tangles, and chronic neuroinflammation. Emerging evidence suggests that the PD-L1/PD-1 immune checkpoint pathway plays a critical role in modulating neuroinflammation, microglial function, and amyloid-β clearance in AD. This review summarizes the current understanding of the PD-L1/PD-1 pathway in AD and discusses its potential as a therapeutic target. Preclinical studies and clinical trials have demonstrated that targeting the PD-L1/PD-1 axis can enhance microglial phagocytosis, promote amyloid-β clearance, and reduce neuroinflammation. We examine the potential benefits and challenges of using existing immunotherapy drugs, such as anti-PD-L1 and anti-PD-1 antibodies, in the context of AD. </p> Additionally, we explore the development of novel, more specific agents targeting the PDL1/ PD-1 pathway, as well as potential synergistic approaches with other immunomodulatory or amyloid-β-targeting treatments. This review provides a comprehensive and up-to-date analysis of the PD-L1/PD-1 immune checkpoint pathway's role in Alzheimer's disease, highlighting its promising therapeutic potential for improving patient outcomes. Further research is warranted to optimize treatment strategies and evaluate the long-term safety and efficacy of targeting this axis in clinical settings.]]></description> </item><item><title><![CDATA[Cachexia: Unraveling its Complex Pathophysiology and Novel Therapeutic Approaches]]></title><link>https://www.benthamscience.com/article/147869</link><pubDate>2026-06-03</pubDate><description><![CDATA[Cachexia is a complex, multifactorial syndrome marked by progressive weight loss, muscle wasting, and metabolic disturbances. It presents significant challenges in clinical practice and contributes to 20% of all cancer-related deaths. While cachexia is commonly linked to cancer, it is also associated with a range of chronic conditions, including chronic heart failure, chronic kidney disease, and autoimmune disorders. Additionally, cachexia is not limited to cancer. Still, it can also occur in end-stage or chronic diseases such as AIDS, chronic obstructive pulmonary disease (COPD), rheumatoid arthritis, tuberculosis, and gastrointestinal diseases. This article aims to explore the intricate pathophysiological mechanisms underlying cachexia and discuss emerging therapeutic strategies for its management. This comprehensive review of the literature and clinical studies explores the intricate interactions between inflammation, disrupted metabolism, hormonal imbalances, and immune dysfunction in cachexia. Furthermore, this review highlights the importance of early detection and intervention in improving the devastating consequences of cachexia on patient outcomes. Finally, this review presents the latest advancements in therapeutic approaches, including pharmacological interventions, nutritional support, exercise regimens, and novel targeted therapies, while underscoring the need for multidisciplinary and personalized treatment strategies.]]></description> </item><item><title><![CDATA[Dendrimers: Advancing Therapeutic Strategies for Dementia]]></title><link>https://www.benthamscience.com/article/150366</link><pubDate>2026-06-03</pubDate><description><![CDATA[Dementia, characterized by a progressive decline in cognitive function, poses a significant challenge to global healthcare systems, with current therapeutic approaches offering limited efficacy. The development of nanotechnology-based drug delivery systems has introduced promising avenues for enhancing the treatment of neurodegenerative disorders such as Alzheimer’s disease. Dendrimers, with their highly branched, nanoscale structure, provide an innovative platform for targeted drug delivery to the brain. Dendrimers serve as nanoscale drug carriers that facilitate controlled drug release, enhance bioavailability, and improve penetration across the blood-brain barrier (BBB), leading to superior therapeutic efficacy in neurodegenerative disorders. In particular, dendrimers can encapsulate both hydrophilic and hydrophobic drugs, increasing their stability and minimizing systemic side effects. This review explores the unique properties of dendrimers, focusing on their potential as drug delivery vehicles in dementia treatment. We also highlight advancements in the design and application of dendrimer-based therapeutics, emphasizing their role in targeting key pathological mechanisms underlying dementia. Through these approaches, dendrimers represent a promising strategy for developing more effective and personalized treatment modalities for patients suffering from cognitive impairment and dementia.]]></description> </item><item><title><![CDATA[Advances in Nanotechnology for Targeted Drug Delivery in Alzheimer's Disease]]></title><link>https://www.benthamscience.com/article/150104</link><pubDate>2026-06-03</pubDate><description><![CDATA[Alzheimer's Disease (AD) is a complex neurodegenerative disorder characterized by progressive cognitive decline and hallmark pathological features, such as amyloid-beta plaques and tau protein tangles. Despite substantial research, current therapeutic strategies remain primarily symptomatic, with limited success in preventing or reversing disease progression. One major challenge is the Blood-Brain Barrier (BBB), which restricts the delivery of therapeutic agents to the brain. Nanotechnology provides innovative solutions to these challenges by enabling the development of targeted drug delivery systems tailored to AD’s unique pathophysiology. Nanoparticles offer several advantages for AD therapy, including their small size, surface modifiability, and the ability to traverse the BBB. These carriers can enhance drug stability, prolong systemic circulation, and enable controlled drug release, reducing systemic toxicity while maximizing therapeutic efficacy. Among various approaches, nanoparticles functionalized with ligands targeting AD show promise in promoting the clearance of pathological aggregates, potentially slowing disease progression and alleviating neurotoxicity. Liposomes, polymeric nanoparticles, dendrimers, and exosomes are notable nanocarriers that have been successfully engineered to deliver a range of therapeutic agents, including anti-amyloid drugs, neuroprotective compounds, and gene therapies. Recent advancements also emphasize stimulus-responsive nanocarriers that release drugs in response to specific pathological cues, further enhancing treatment precision. This article delves into the most recent advancements in nanotechnology for AD therapy, and the potential of these innovative systems to overcome long-standing barriers in AD treatment and paving the way for more effective and targeted interventions.]]></description> </item><item><title><![CDATA[Unravelling the Association between FOXO3a and Cancer Cell Senescence: An Insight into its Role and Biological Pathway]]></title><link>https://www.benthamscience.com/article/150826</link><pubDate>2026-06-03</pubDate><description><![CDATA[This review explores the intricate relationship between FOXO3a and cellular senescence in cancer, highlighting its complex and context-dependent function. FOXO3a, a transcription factor commonly known as a tumor suppressor, exhibits paradoxical roles in cancer biology. This review describes FOXO3a's dual functions in promoting tumor suppression and progression, its interplay with senescence pathways, and its impact on cancer cell phenotypes. Senescence is also known to be a tumor suppressor and a barrier against malignancies. However, persistent senescence has been found to create an adverse effect due to cancer progression and therapeutic endeavors. The review also discusses the potential of senescence management and FOXO3a modulation as novel therapeutic strategies in cancer treatment. Recent advancements in proteomics research, including FOXO3a's interactions with microRNAs, post-translational modifications, and protein-protein interactions, are also elaborated. This paper concludes by emphasizing the need to understand the role of FOXO3a in cancer biology and its potential as a biomarker and therapeutic target.]]></description> </item><item><title><![CDATA[Hybrid Cosmeceutical Innovations for Aging Skin: Bridging Functional Skincare and Therapeutic Benefits through Multifunctional Formulations]]></title><link>https://www.benthamscience.com/article/150632</link><pubDate>2026-06-03</pubDate><description><![CDATA[A new generation of hybrid cosmetics has come into existence, providing an efficient means to achieve both skincare and aesthetic objectives with only one product. These cosmetics incorporate ingredients from natural and synthetic sources, making use of cutting-edge technologies to improve efficacy, sustainability, and customer pleasure. This review paper will focus on the effects of hybrid cosmetics on different types of skin cells, the technologies employed, and the role of ingredients like botanical extracts, marine-based active ingredients, and synthetic compounds in the cosmetic formulations, in order to provide improved skincare benefits. Various technologies like nanotechnology, encapsulation technique, transdermal patches, electroporation, and iontophoresis are analyzed for their role in enhancing efficacy and sustainability. Hybrid cosmetics containing natural ingredients of marine origin, like Laminaria japonica and Pseudopterogorgia elisabethae, as well as botanical extracts like Resveratrol, provide safe, ecofriendly, and sustainable cosmetics, whereas synthetically derived compounds that are used in the cosmetic industry, like Hyaluronic acid and Niacinamide, provide quick action and targeted delivery. The findings of this review suggest novel dual approaches for developing a range of hybrid products to meet the increasing needs of consumers, as well as techniques for improving stability and efficacy. Using natural ingredients aligns with the growing trend toward sustainability in cosmetics. Synthetic ingredients have been developed for precise delivery, rapid action, and affordability. However, by implementing appropriate strategies for technology and ingredient selection, consumers' demands for effective products can be met.]]></description> </item><item><title><![CDATA[Advancing Mitochondrial Health in Huntington Disease (HD): Small Molecule Therapies and Neurodegeneration]]></title><link>https://www.benthamscience.com/article/150508</link><pubDate>2026-06-03</pubDate><description><![CDATA[Huntington's disease (HD) is a severe neurodegenerative disorder caused by an expanded CAG repeat in the huntingtin gene, leading to the production of a mutant huntingtin protein. This mutation results in progressive motor, cognitive, and psychiatric impairments, alongside significant neuronal loss. Mitochondrial dysfunction plays a pivotal role in the pathophysiology of HD, contributing to disease progression and neuronal death. This article aims to evaluate small molecule-based therapeutic strategies designed to enhance mitochondrial function as a potential approach to alleviate symptoms and slow the progression of HD and related neurodegenerative disorders. A comprehensive review of recent literature is conducted to identify small molecules targeting mitochondrial dysfunction from Google Scholar, Pub- Med/Medline/PMC, ScienceDirect, Elsevier, Google Patents, and Clinicaltrials.gov.in, among others. The analysis focuses on their mechanisms of action, including reducing oxidative stress, enhancing mitochondrial biogenesis, and improving mitochondrial dynamics and function. The review identifies several promising small molecules capable of targeting mitochondrial dysfunction. These agents demonstrate potential in preclinical studies to alleviate HD symptoms and modify disease progression by addressing key aspects of mitochondrial health. Small molecule therapies targeting mitochondrial dysfunction offer considerable promise for treating HD. However, further research is required to optimize these therapies for clinical use and to evaluate their long-term impact on disease progression to fully establish their therapeutic efficacy.]]></description> </item><item><title><![CDATA[Synergistic Enhancement of Anti-aging Effects on Human Umbilical Vein Endothelial Cells Treated With the Combination of Ferulic Acid and Rapamycin]]></title><link>https://www.benthamscience.com/article/150078</link><pubDate>2026-06-03</pubDate><description><![CDATA[<p> Introduction: Aging is a complex process involving cellular, genetic, metabolic, and mitochondrial changes. While significant progress has been made in understanding aging mechanisms and developing anti-aging drugs, single-drug treatments have limitations. This paper aims to investigate the synergistic effects of Ferulic acid (FA) and Rapamycin (Rapa) on anti-aging and to elucidate their underlying mechanisms, providing novel strategies for future anti-aging therapies. </p><p> Methods: The safe concentration ranges of FA and Rapa for Human umbilical vein endothelial cells (HUVECs) were determined via Cell counting kit (CCK-8) and Senescence-associated β- Gal staining, with EC50 calculated by GraphPad Prism 8.0.2. Effects on cell cycle arrest and ROS in D-gal-induced aging HUVECs were assessed, with synergistic mechanisms explored by Western Blot and RT-qPCR for aging markers, inflammatory factors, and fibrosis genes. </p><p> Results: CCK-8 showed that 20-160 μM FA and 50-200 pM Rapa enhanced HUVECs proliferation, with EC50 of 37.78 μM for FA and 48.32 pM for Rapa. The optimal 1:2 combination ratio demonstrated reduced G0/G1 cells, decreased ROS, and lowered NF-κB p65, p53, IL-1β, and TNF-α expression. It also inhibited fibrosis-related gene transcription, downregulating aging markers and maintaining cellular homeostasis. </p><p> Discussion: These results align with previous studies highlighting FA’s antioxidant properties and Rapa’s role in mTOR inhibition, suggesting that their combination targets multiple aging pathways simultaneously. The dual approach—reducing oxidative damage while modulating inflammation and fibrosis—may offer superior efficacy compared to single-drug interventions. </p><p> Conclusion: In summary, this dual-target strategy presents a promising avenue for developing advanced anti-aging therapies, warranting further investigation in preclinical and clinical settings. </p>]]></description> </item></channel></rss>