Healthy ageing and longevity, Год журнала: 2024, Номер unknown, С. 255 - 275
Опубликована: Янв. 1, 2024
Язык: Английский
Healthy ageing and longevity, Год журнала: 2024, Номер unknown, С. 255 - 275
Опубликована: Янв. 1, 2024
Язык: Английский
The Egyptian Journal of Internal Medicine, Год журнала: 2025, Номер 37(1)
Опубликована: Янв. 24, 2025
Abstract This narrative review explores the relationship between air pollution and neurodegenerative diseases (NDs). Historically, has been linked primarily to respiratory cardiovascular issues, but recent evidence suggests that it may also impact neurological health. With global increase in diseases, understanding environmental risk factors become crucial. The synthesizes findings from studies, highlighting potential role of pollutants—particularly fine particulate matter (PM2.5), ozone, nitrogen dioxide (NO2), heavy metals—in onset progression NDs. Key mechanisms under investigation include brain inflammation microglial activation, which are believed contribute processes. Animal human studies have shown correlations exposure increased cognitive decline disorders. Research indicates exacerbate neuroinflammation cause white abnormalities, disrupt neural communication function. Additionally, emerging like residential greenness climate action could mitigate some these adverse effects. Despite advancements, significant knowledge gaps remain, particularly regarding long-term chronic specific molecular pathways involved. shows need for further research clarify develop targeted interventions. Addressing pollution’s on requires comprehensive public health strategies, including stricter regulations awareness, alongside continued into preventive therapeutic measures.
Язык: Английский
Процитировано
6Pharmaceuticals, Год журнала: 2025, Номер 18(1), С. 104 - 104
Опубликована: Янв. 15, 2025
Cytokine-mediated inflammation is increasingly recognized for playing a vital role in the pathophysiology of wide range brain disorders, including neurodegenerative, psychiatric, and neurodevelopmental problems. Pro-inflammatory cytokines such as interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) cause neuroinflammation, alter function, accelerate disease development. Despite progress understanding these pathways, effective medicines targeting are still limited. Traditional anti-inflammatory immunomodulatory drugs peripheral inflammatory illnesses. Still, they face substantial hurdles when applied to central nervous system (CNS), blood-brain barrier (BBB) unwanted systemic effects. This review highlights developing treatment techniques modifying cytokine-driven focusing on advances that selectively target critical involved pathology. Novel approaches, cytokine-specific inhibitors, antibody-based therapeutics, gene- RNA-based interventions, sophisticated drug delivery systems like nanoparticles, show promise with respect lowering neuroinflammation greater specificity safety. Furthermore, developments biomarker discoveries neuroimaging improving our ability monitor responses, allowing more accurate personalized regimens. Preclinical clinical trial data demonstrate therapeutic potential tailored techniques. However, significant challenges remain, across BBB reducing off-target As research advances, creation personalized, cytokine-centered therapeutics has therapy landscape illnesses, giving patients hope better results higher quality life.
Язык: Английский
Процитировано
2Aging Cell, Год журнала: 2025, Номер unknown
Опубликована: Апрель 23, 2025
ABSTRACT Human aging presents an evolutionary paradox: while rates remain constant, healthspan and lifespan vary widely. We address this conundrum via salutogenesis—the active production of health—through immune resilience (IR), the capacity to resist disease despite inflammation. Analyzing ~17,500 individuals across stages inflammatory challenges, we identified a core salutogenic mechanism: IR centered on TCF7 , conserved transcription factor maintaining T‐cell stemness regenerative potential. integrates innate adaptive immunity counter three mortality drivers: chronic inflammation (inflammaging), aging, cellular senescence. By mitigating these mechanisms, confers survival advantages: At age 40, with poor face 9.7‐fold higher rate—a risk equivalent that 55.5‐year‐olds optimal IR—resulting in 15.5‐year gap survival. Optimal preserves youthful profiles at any age, enhances vaccine responses, reduces burdens cardiovascular disease, Alzheimer's, serious infections. Two key themes emerge: first, female‐predominant IR, including likely reflects pressures favoring reproductive success caregiving; second, midlife (40–70 years) is critical window where by 69%. After 70, converge between resilient non‐resilient groups, reflecting biological limits longevity extension. TNFα‐blockers restore salutogenesis pathways, indicating delays aging‐related processes rather than altering rates. reframing as salutogenic‐pathogenic balance, establish ‐centered central healthy longevity. Targeted interventions enhance offer actionable strategies maximize before constraints limit benefits.
Язык: Английский
Процитировано
2Brain Sciences, Год журнала: 2023, Номер 14(1), С. 19 - 19
Опубликована: Дек. 23, 2023
The term “neuroinflammation” defines the typical inflammatory response of brain closely related to onset many neurodegenerative diseases (NDs). Neuroinflammation is well known, but its mechanisms and pathways are not entirely comprehended. Some progresses have been achieved through efforts research. Consequently, new cellular molecular mechanisms, diverse conventional, emerging. In listing some those that will be subject our description discussion, essential important roles peripheral infiltrated monocytes clonotypic cells, alterations in gut–brain axis, dysregulation apelinergic system, endothelial glycocalyx component neuronal vascular units, variations expression genes levels encoding molecules by action microRNAs (miRNAs), or other epigenetic factors distinctive transcriptional factors, as role autophagy, ferroptosis, sex differences, modifications circadian cycle. Such can add significantly understanding complex etiological puzzle neuroinflammation ND. addition, they could represent biomarkers targets ND, which increasing elderly.
Язык: Английский
Процитировано
23Molecular Neurobiology, Год журнала: 2024, Номер unknown
Опубликована: Сен. 4, 2024
Язык: Английский
Процитировано
8Frontiers in Aging Neuroscience, Год журнала: 2024, Номер 16
Опубликована: Авг. 21, 2024
Introduction Alzheimer’s disease (AD), a major cause of dementia globally, imposes significant societal and personal costs. This review explores the efficacy physical exercise as non-pharmacological intervention to mitigate impacts AD. Methods draws on recent studies that investigate effects neuroinflammation neuronal enhancement in individuals with Results Consistent alters neuroinflammatory pathways, enhances cognitive functions, bolsters brain health among AD patients. It favorably influences activation states microglia astrocytes, fortifies integrity blood-brain barrier, attenuates gut inflammation associated These changes are substantial improvements performance indicators. Discussion The findings underscore potential integrating into comprehensive management strategies. Emphasizing necessity for further research, this advocates refinement regimens maximize their enduring benefits decelerating progression
Язык: Английский
Процитировано
5Опубликована: Ноя. 27, 2023
With the term neuroinflammation has defined typical inflammatory response of brain closely related to onset many neurological diseases. Neuroinflammation is well known, but its mechanisms and pathways are not entirely comprehended. Currently, some progress been achieved through efforts research. Consequently, new cellular molecular mecha-nisms, diverse from conventional ones, emerging. In listing those that will be sub-ject our description discussion, essential important role peripheral infiltrated monocytes clonotypic cells, alterations in gut/brain axis, dysregulation apelinergic sys-tem, as changes endothelial glycocalyx blood-brain barrier, variation expres-sion genes levels encoding molecules by microRNAs (miRNAs), or other epige-netic factors distinctive transcriptional factors, autophagy, ferroptosis, sex differences modifications circadian cycle. Such mentioned can add significant pieces understanding complex etiological puzzle neuroinflammation. addi-tion, they could represent biomarkers targets neurodegenerative diseases, increase old populations.
Язык: Английский
Процитировано
10Toxicology and Applied Pharmacology, Год журнала: 2024, Номер 492, С. 117085 - 117085
Опубликована: Сен. 3, 2024
The significant rise in cancer survivorship stands out as one of the most notable achievements modern science. However, this comes with a burden, treatment is not without adverse effects. Lately, there has been growing focus on cognitive dysfunction associated treatment, often referred to 'chemobrain'. It significantly impacts quality life for survivors. underlying mechanisms studied so far usually neurons, while other cells central nervous system are overlooked. This review seeks place hypothesis that glial may play role development chemotherapy-induced dysfunction. summarizes primary proposed date underscoring existing gaps research field. Inflammation and release pro-inflammatory mediators by M1 microglia A1 astrocytes prevalent finding after chemotherapy. activation some chemotherapeutic agents contribute neuronal degeneration, alterations synaptic branches, well glutamate excitotoxicity, which can impairment. reduction number oligodendrocytes chemotherapy also impact myelin sheath, contributing Furthermore, drugs activate microglia, decreased neuroplasticity and, possibly, In conclusion, data regarding effects scarce, it essential understand how these affected enable reliable therapeutic or preventive actions cancer-treated patients.
Язык: Английский
Процитировано
3Journal of Alzheimer s Disease, Год журнала: 2024, Номер unknown
Опубликована: Ноя. 18, 2024
Several studies indicate that the development of Alzheimer's disease (AD) has strong interactions with immune mechanisms within brain, indicating a close association between inflammation in central nervous system and progression neurodegeneration. Despite considerable progress understanding inflammatory aspects AD, several them remain unresolved. Pro-inflammatory cytokines microglia are pivotal components cascade. Among these, role interleukin-8 (IL-8) neurodegeneration seems complex multifaceted, involving inflammation, neurotoxicity, blood-brain barrier disruption, oxidative stress, is still poorly characterized. We conducted review to describe evidence IL-8 involvement AD. cytokine known for its proinflammatory properties typically produced by macrophages, predominantly functions as chemotactic signal attracting neutrophils inflamed sites bloodstream. Interestingly, also present where it primarily released response signals. This aims provide comprehensive overview structure, function, regulatory relevant AD pathology.
Язык: Английский
Процитировано
3Small, Год журнала: 2025, Номер 21(9)
Опубликована: Янв. 22, 2025
Abstract Nanomaterials with unparalleled physical and chemical attributes have become a cornerstone in the field of nanomedicine delivery. These materials can be engineered into various functionalized nanocarriers, which focus research. Stimulus‐responsive nanodrug delivery systems (SRDDS) stand out as sophisticated class nanocarriers that release drugs response to environmental cues. Due complex pathogenesis multifaceted pathological environment nervous system, developing accurate effective drug therapy low side‐effects is formidable task. In recent years, SRDDS been widely used treatment neurological diseases. By customizing align specific microenvironment system tissues or external stimulation, efficacy enhanced. This review provides an in‐depth look at characteristics diseases highlights case studies tailored treat these disorders based on unique stimulation criteria triggers. Additionally, this comprehensive overview progress future prospects technology diseases, providing valuable guidance for its transition from fundamental research clinical application.
Язык: Английский
Процитировано
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