Ageing Research Reviews, Год журнала: 2024, Номер 101, С. 102535 - 102535
Опубликована: Окт. 6, 2024
Язык: Английский
Journal of Translational Medicine, Год журнала: 2025, Номер 23(1)
Опубликована: Янв. 15, 2025
Язык: Английский
Процитировано
2
RSC Advances, Год журнала: 2024, Номер 14(16), С. 11057 - 11088
Опубликована: Янв. 1, 2024
Alzheimer has many crucial factors that should be considered in order to get better results from clinical trials. Benzimidazole and its isosteres represent significant scaffolds for designing potential multi-target anti-alzheimer molecules.
Язык: Английский
Процитировано
15
Metabolic Brain Disease, Год журнала: 2025, Номер 40(2)
Опубликована: Фев. 1, 2025
The central nervous system (CNS) is immune-privileged by several immuno-modulators as interleukins (ILs). ILs are cytokines secreted immune cells for cell-cell signaling communications and affect the functions of CNS. were reported to orchestrate different molecular cellular mechanisms both physiological pathological events, through overproduction or over-expression their receptors. They interact with numerous receptors mediating pro-inflammatory and/or anti-inflammatory actions. Interleukins have been implicated participate in neurodegenerative diseases. play a critical role Alzheimer's disease (AD) pathology which characterized over-production ILs. These may aggravate neurodegeneration, addition contribution detrimental oxidative stress, excitotoxicity. However, recent research on relation between AD revealed major discrepancies. Most shown pro- roles experimental settings models. interactions shared pathways also add difficulty drawing solid conclusions. In addition, targeting has not yielded consistent results. repeated failures therapeutic drugs treating necessitate search novel agents multiple pathology. this context, understanding throughout progression interaction other systems brain provide promising targets prevention treatment AD.
Язык: Английский
Процитировано
1
Biomolecules, Год журнала: 2024, Номер 14(7), С. 833 - 833
Опубликована: Июль 11, 2024
Microglia, as resident macrophages in the central nervous system, play a multifunctional role pathogenesis of Alzheimer’s disease (AD). Their clustering around amyloid-β (Aβ) deposits is core pathological feature AD. Recent advances single-cell RNA sequencing (scRNA-seq) and single-nucleus (snRNA-seq) have revealed dynamic changes microglial phenotypes over time across different brain regions during aging AD progression. As advances, microglia primarily exhibit impaired phagocytosis Aβ tau, along with release pro-inflammatory cytokines that damage synapses neurons. Targeting has emerged potential therapeutic approach for Treatment strategies involving can be broadly categorized into two aspects: (1) enhancing function: This involves augmenting their phagocytic ability against cellular debris (2) mitigating neuroinflammation: Strategies include inhibiting TNF-α signaling to reduce neuroinflammatory response triggered by microglia. Clinical trials exploring microglia-related approaches treatment garnered attention. Additionally, natural products show promise beneficial effects suppressing inflammatory responses. Clarifying dynamics, understanding roles, novel will advance our fight
Язык: Английский
Процитировано
7
Frontiers in Immunology, Год журнала: 2024, Номер 15
Опубликована: Апрель 4, 2024
Aging is a complex process characterized by myriad of physiological changes, including alterations in the immune system termed immunosenescence. It exerts profound effects on both bone marrow and central nervous system, with significant implications for immunosenescence neurological contexts. Our mini-review explores relationship between aging its impact immunosenescence, specifically within context diseases. The serves as crucial hub hematopoiesis cell production, yet age, it undergoes alterations, hematopoietic stem function, niche composition, inflammatory signaling. These age-related shifts microenvironment contribute to dysregulation homeostasis impacting neuroinflammatory processes neuronal health. In our review, we aim explore cellular molecular mechanisms that link inflammaging, neuroinflammation, specific focus their relevance pathophysiology disorders. By exploring this interplay, strive provide comprehensive understanding how impacts function contributes progression diseases individuals. Ultimately, knowledge can hold substantial promise development innovative therapeutic interventions aimed at preserving mitigating disorders elderly population.
Язык: Английский
Процитировано
5
International Immunopharmacology, Год журнала: 2024, Номер 135, С. 112328 - 112328
Опубликована: Май 25, 2024
Язык: Английский
Процитировано
5
International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(13), С. 6928 - 6928
Опубликована: Июнь 25, 2024
Air pollution, a growing concern for public health, has been linked to various respiratory and cardiovascular diseases. Emerging evidence also suggests link between exposure air pollutants neurodegenerative diseases, particularly Alzheimer's disease (AD). This review explores the composition sources of pollutants, including particulate matter, gases, persistent organic heavy metals. The pathophysiology AD is briefly discussed, highlighting role beta-amyloid plaques, neurofibrillary tangles, genetic factors. article examines how reach brain exert their detrimental effects, delving into neurotoxicity pollutants. molecular mechanisms linking pollution neurodegeneration are explored in detail, focusing on oxidative stress, neuroinflammation, protein aggregation. Preclinical studies, vitro experiments animal models, provide direct effects neuronal cells, glial blood-brain barrier. Epidemiological studies have reported associations an increased risk cognitive decline. body supporting as modifiable factor underscores importance considering environmental factors etiology progression face worsening global quality.
Язык: Английский
Процитировано
5
Cells, Год журнала: 2024, Номер 13(4), С. 309 - 309
Опубликована: Фев. 7, 2024
Alzheimer’s disease (AD), marked by cognitive impairment, predominantly affects the brain regions regulated cholinergic innervation, such as cerebral cortex and hippocampus. Cholinergic dysfunction, a key contributor to age-related decline, has spurred investigations into potential therapeutic interventions. We have previously shown that choline alphoscerate (α-GPC), neurotransmission-enhancing agent, protects from Aβ-mediated neurotoxicity. Herein, we investigated effects of α-GPC on microglial phenotype in response Aβ via modulation nicotinic alpha-7 acetylcholine receptor (α7 nAChR). BV2 cells were pre-treated for 1 h with treated 24, 48, 72 Aβ1–42 and/or α-BTX, selective α7nAchR antagonist. Fluorescent immunocytochemistry Western blot analysis showed was able antagonize Aβ-induced inflammatory effects. Of note, exerted its anti-inflammatory effect directly activating α7nAChR receptor, suggested induction an increase [Ca2+]i Ach-like currents. Considering transmission appears crucial regulating profiles glial cells, emerges pharmaco-therapeutic target improve outcomes neurodegenerative disorders, AD.
Язык: Английский
Процитировано
4
Frontiers in Pharmacology, Год журнала: 2024, Номер 15
Опубликована: Июль 29, 2024
Alzheimer's disease (AD) and other forms of dementia have a devastating effect on the community healthcare system, as neurodegenerative diseases are causing disability dependency in older population. Pharmacological treatment options limited to symptomatic alleviation cholinergic deficit accelerated clearance β-amyloid aggregates, but accessible disease-modifying interventions needed especially early phase AD. Melatonin was previously demonstrated improve cognitive function clinical setting experimental studies also.
Язык: Английский
Процитировано
4
Biomedicines, Год журнала: 2025, Номер 13(1), С. 103 - 103
Опубликована: Янв. 5, 2025
Heparan sulfate (HS) is a polysaccharide that found on the surface of cells and has various biological functions in body. The purpose this study was to predict pharmacological effects molecular mechanisms HS Alzheimer's disease (AD) neuroinflammation (NI) through network pharmacology analysis experimentally verify them. We performed functional enrichment common genes between target AD-NI gene sets obtained items such as "Cytokine-Mediated Signaling Pathway", "Positive Regulation Of MAPK Cascade", "MAPK signaling pathway". To confirm predicted results, anti-inflammatory effect investigated using lipopolysaccharide (LPS)-stimulated BV2 microglia cells. inhibited production nittic oxide, interleukin (IL)-6, tumor necrosis factor-α LPS-stimulated cells, but not IL-1β. In addition, inactivated P38 pathway. These findings suggest potential for become new treatment AD NI.
Язык: Английский
Процитировано
0