Elsevier eBooks, Год журнала: 2025, Номер unknown, С. 289 - 314
Опубликована: Янв. 1, 2025
Язык: Английский
Elsevier eBooks, Год журнала: 2025, Номер unknown, С. 289 - 314
Опубликована: Янв. 1, 2025
Язык: Английский
Ageing Research Reviews, Год журнала: 2024, Номер 99, С. 102357 - 102357
Опубликована: Июнь 1, 2024
Neurodegenerative disorders (NDs) are expected to pose a significant challenge for both medicine and public health in the upcoming years due global demographic changes. NDs mainly represented by degeneration/loss of neurons, which is primarily accountable severe mental illness. This neuronal degeneration leads many neuropsychiatric problems permanent disability an individual. Moreover, tight junction brain, blood-brain barrier (BBB)has protective feature, functioning as biological that can prevent medicines, toxins, foreign substances from entering brain. However, delivering any medicinal agent brain (i.e., Multiple sclerosis, Alzheimer's, Parkinson's, etc.) enormously challenging. There approved therapies address NDs, but most them only help treat associated manifestations. The available have failed control progression certain factors, i.e., BBB drug-associated undesirable effects. extremely complex pathology, with pathogenic mechanisms involved initiation progression; thereby, limited survival rate has been observed ND patients. Hence, understanding exact mechanism behind crucial developing alternative approaches improving patients' rates. Thus, present review sheds light on different cellular novel therapeutic their clinical relevance, will assist researchers alternate strategies limitations conventional therapies. current work offers scope into near future improve approach NDs.
Язык: Английский
Процитировано
28Journal of Neuroinflammation, Год журнала: 2024, Номер 21(1)
Опубликована: Фев. 2, 2024
Abstract Neuroinflammation is a pathological hallmark of Alzheimer’s disease (AD), characterized by the stimulation resident immune cells brain and penetration peripheral cells. These inflammatory processes facilitate deposition amyloid-beta (Aβ) plaques abnormal hyperphosphorylation tau protein. Managing neuroinflammation to restore homeostasis decrease neuronal damage therapeutic approach for AD. One way achieve this through exercise, which can improve function protect against neuroinflammation, oxidative stress, synaptic dysfunction in AD models. The neuroprotective impact exercise regulated various molecular factors that be activated same as administration their mimetics. Recent evidence has proven some mimetics effective alleviating AD, and, additionally, they are helpful alternative option patients who unable perform regular physical manage neurodegenerative disorders. This review focuses on current state knowledge mimetics, including efficacy, regulatory mechanisms, progress, challenges, limitations, future guidance application therapy.
Язык: Английский
Процитировано
19Intelligent Pharmacy, Год журнала: 2024, Номер unknown
Опубликована: Сен. 1, 2024
Язык: Английский
Процитировано
18Nutrients, Год журнала: 2022, Номер 14(19), С. 4134 - 4134
Опубликована: Окт. 5, 2022
Neuroinflammation occurs throughout the pathogenesis of Alzheimer's disease (AD). Here, we investigated effects treadmill exercise on neuroinflammation in APP/PS1 transgenic AD mice and potential involvement microbe-gut-brain axis (MGB) mechanisms based growing evidence that AD's is correlated with a deterioration function gut microbiota. were subjected to 12 weeks exercise, followed by spatial memory tests. After behavioral study, amyloid (Aβ) pathology, microbes metabolites, bacterial lipopolysaccharide (LPS) displacement, degree analyzed. We found this strategy enriched microbial diversity alleviated brain. Notably, led reductions pathogenic bacteria such as intestinal Allobaculum, increases probiotic Akkermansia, increased levels intestine-brain barrier proteins, attenuated LPS displacement. These results suggest prolonged can effectively modulate thereby reduce displacement ultimately alleviate AD-related neuroinflammation.
Язык: Английский
Процитировано
46International Journal of Molecular Sciences, Год журнала: 2023, Номер 24(6), С. 5283 - 5283
Опубликована: Март 9, 2023
The blood-brain barrier (BBB) is a functional interface that provides selective permeability, protection from toxic substances, transport of nutrients, and clearance brain metabolites. Additionally, BBB disruption has been shown to play role in many neurodegenerative conditions diseases. Therefore, the aim this study was establish functional, convenient, efficient vitro co-cultured model can be used for several physiological related disruption. Mouse brain-derived endothelial (bEnd.3) astrocyte (C8-D1A) cells were on transwell membranes an intact model. its effects different neurological diseases stress conditions, including Alzheimer's disease (AD), neuroinflammation, obesity, have examined by transendothelial electrical resistance (TEER), fluorescein isothiocyanate (FITC) dextran, tight junction protein analyses. Scanning electron microscope images showed evidence end-feet processes passing through membrane transwell. Moreover, effective properties TEER, FITC, solvent persistence leakage tests when compared mono-cultured immunoblot results expression proteins such as zonula occludens-1 (ZO-1), claudin-5, occludin-1 enhanced co-culture. Lastly, under structural integrity decreased. present demonstrated mimicked BBB's and, similar damages. convenient experimental tool investigate wide range BBB-related pathological studies.
Язык: Английский
Процитировано
34International Journal of Molecular Sciences, Год журнала: 2023, Номер 24(6), С. 5383 - 5383
Опубликована: Март 11, 2023
Alzheimer’s disease (AD) is an incurable, progressive neurodegenerative disorder. AD a complex and multifactorial that responsible for 60–80% of dementia cases. Aging, genetic factors, epigenetic changes are the main risk factors AD. Two aggregation-prone proteins play decisive role in pathogenesis: β-amyloid (Aβ) hyperphosphorylated tau (pTau). Both them form deposits diffusible toxic aggregates brain. These biomarkers Different hypotheses have tried to explain pathogenesis served as platforms drug research. Experiments demonstrated both Aβ pTau might start processes necessary cognitive decline. The two pathologies act synergy. Inhibition formation has been old target. Recently, successful clearance by monoclonal antibodies raised new hopes treatments if detected at early stages. More recently, novel targets, e.g., improvements amyloid from brain, application small heat shock (Hsps), modulation chronic neuroinflammation different receptor ligands, microglial phagocytosis, increase myelination revealed
Язык: Английский
Процитировано
23Journal of Biophotonics, Год журнала: 2025, Номер unknown
Опубликована: Янв. 22, 2025
ABSTRACT Neuroinflammation plays a key role in the development of neurodegenerative diseases, with microglia regulating this process through pro‐inflammatory M1 and anti‐inflammatory M2 phenotypes. Studies have shown that human umbilical cord mesenchymal stem cells (hUCMSCs) modulate neuroinflammation by secreting cytokines. Photobiomodulation (PBM), non‐invasive therapy, has demonstrated significant potential alleviating neuroinflammation. This study examines combined effects PBM hUCMSCs an vitro microglial inflammation model LPS‐induced mouse model. The results show PBM‐pretreated promoted polarization improved cognitive function mice downregulating Notch signaling pathway, suggesting promising new approach for treating diseases.
Язык: Английский
Процитировано
1International Journal of Nanomedicine, Год журнала: 2023, Номер Volume 18, С. 4193 - 4227
Опубликована: Июль 1, 2023
Introduction: Donepezil (DPL), a specific acetylcholinesterase inhibitor, is used as first-line treatment to improve cognitive deficits in Alzheimer's disease (AD) and it might have modifying effect. Astaxanthin (AST) natural potent antioxidant with neuroprotective, anti-amyloidogenic, anti-apoptotic, anti-inflammatory effects. This study aimed prepare nanostructured lipid carriers (NLCs) co-loaded donepezil astaxanthin (DPL/AST–NLCs) evaluate their vivo efficacy an AD-like rat model 30 days after daily intranasal administration. Methods: DPL/AST–NLCs were prepared using hot high-shear homogenization technique, vitro examined for physicochemical parameters evaluated. AD induction rats was performed by aluminum chloride. The cortex hippocampus isolated from the brain of biochemical testing histopathological examination. Results: showed z-average diameter 149.9 ± 3.21 nm, polydispersity index 0.224 0.017, zeta potential – 33.7 4.71 mV, entrapment efficiency 81.25 1.98% (donepezil) 93.85 1.75% (astaxanthin), sustained release both 24 h, spherical morphology transmission electron microscopy, they stable at 4– 8 2°C six months. Differential scanning calorimetry revealed that molecularly dispersed NLC matrix amorphous state. DPL/AST–NLC-treated significantly lower levels nuclear factor-kappa B, malondialdehyde, β-site amyloid precursor protein cleaving enzyme-1, caspase-3, beta (Aβ 1‑42 ), acetylcholinesterase, higher glutathione acetylcholine than untreated treated donepezil–NLCs. antioxidant, anti-acetylcholinesterase, anti-inflammatory, anti-apoptotic effects, resulting significant improvement cortical hippocampal histopathology. Conclusion: Nose-to-brain delivery promising strategy management AD. Keywords: disease, donepezil, astaxanthin, delivery,
Язык: Английский
Процитировано
19Saudi Pharmaceutical Journal, Год журнала: 2023, Номер 31(9), С. 101728 - 101728
Опубликована: Авг. 3, 2023
Neuroinflammation is associated with the elevation of toxic proinflammatory mediators that promote neurodegeneration and subsequently affect cognition. Causes inflammation in neuronal cells are believed to initiate various neurodegenerative disorders, mainly Alzheimer's disease. Levetiracetam a second-generation antiepileptic drug. There evidence supporting memory-enhancing effect levetiracetam from numerous experimental clinical studies. Therefore, this research focused on finding its protective effects against lipopolysaccharides prompted cognitive impairment exploring possible mechanisms underlining their neuroprotection.Two doses (100 or 200 mg/kg) were administrated orally for 30 days. Additionally, four (250 µg/kg) lipopolysaccharide injected peripherally induce neurotoxicity. Behavioral tests carried out using maze models. At end tests, brain tissues collected biochemical evaluations. Cholinergic, neuroinflammatory, apoptosis, oxidative-related parameters analyzed homogenate explore action levetiracetam.In lipopolysaccharide-induced rats, indicated reduction (p < 0.01) transfer latency elevated plus-maze. An improvement novel familiar objects exploration time object recognition test. A rise 0.05) arm entries extended spent Y-maze In extension, levels acetylcholine 0.001), anti-inflammatory factors (transforming growth factor-β1; p 0.01 interleukin-10; 0.05), an antioxidant (catalase; rats after administration levetiracetam. contrast, inflammatory (cyclooxygenase-2; 0.05, nuclear factor kappa B; tumor necrosis factor-α; 0.01, interleukin-6 0.01), apoptosis inducers (BCL2-associated X protein; 0.05 Caspase-3 oxidative stress (malondialdehyde; considerably reduced rats.The collective results suggested may be able treat neuroinflammatory-related memory loss by enhancing cholinergic activity while reducing neuroinflammation, cellular stress.
Язык: Английский
Процитировано
16Pharmaceuticals, Год журнала: 2024, Номер 17(6), С. 701 - 701
Опубликована: Май 28, 2024
Neurodegenerative diseases (Alzheimer’s disease, Parkinson’s Huntington’s and others) cancer, seemingly disparate in their etiology manifestation, exhibit intriguing associations certain cellular molecular processes. Both cancer neurodegenerative involve the deregulation of processes such as apoptosis, proliferation, DNA repair pose a significant global health challenge. Afzelin (kaempferol 3-O-rhamnoside) is flavonoid compound abundant various plant sources. exhibits diverse range biological activities, offering promising prospects for treatment hallmarked by oxidative stress cell death pathways. Its protective potential against also alleviating side effects chemotherapy. This review explores therapeutic implications afzelin, including its capacity to mitigate stress, modulate inflammation, promote regeneration diseases.
Язык: Английский
Процитировано
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