Neuropharmacology, Год журнала: 2024, Номер unknown, С. 110241 - 110241
Опубликована: Ноя. 1, 2024
Язык: Английский
International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(3), С. 1130 - 1130
Опубликована: Янв. 28, 2025
Oxidative stress plays a role in various pathophysiological diseases, including neurogenerative such as Alzheimer′s disease (AD), which is the most prevalent neuro-pathology aging population. has been reported to be one of earliest pathological alterations AD. Additionally, it was demonstrated that older adults, there loss free radical scavenging ability. The Nrf2 transcription factor key regulator antioxidant defense systems, but, with aging, both amount and transcriptional activity decrease. With available treatments for AD being poorly effective, reinforcing systems via pathway may way prevent treat To highlight predominant signaling defending against oxidative and, therefore, neurotoxicity, we present an overview natural compounds exert their own neuroprotective roles through activation pathway. This review opportunity promote holistic approach treatment need further refine development new potential Nrf2-targeting drugs.
Язык: Английский
Процитировано
1
Journal of Clinical Medicine, Год журнала: 2025, Номер 14(2), С. 386 - 386
Опубликована: Янв. 9, 2025
The blood-brain barrier (BBB) is a crucial structure that maintains brain homeostasis by regulating the entry of molecules and cells from bloodstream into central nervous system (CNS). Neurodegenerative diseases such as Alzheimer's Parkinson's disease, well ischemic stroke, compromise integrity BBB. This leads to increased permeability infiltration harmful substances, thereby accelerating neurodegeneration. In this review, we explore mechanisms underlying BBB disruption, including oxidative stress, neuroinflammation, vascular dysfunction, loss tight junction integrity, in patients with neurodegenerative diseases. We discuss how breakdown contributes neurotoxicity, abnormal accumulation pathological proteins, all which exacerbate neuronal damage facilitate disease progression. Furthermore, potential therapeutic strategies aimed at preserving or restoring function, anti-inflammatory treatments, antioxidant therapies, approaches enhance integrity. Given role neurodegeneration, maintaining its represents promising approach slow prevent progression
Язык: Английский
Процитировано
0
Current Opinion in Neurology, Год журнала: 2025, Номер unknown
Опубликована: Фев. 7, 2025
Purpose of review The present aims to provide an overview the existing understanding role gut microbiome in Alzheimer's disease pathophysiology. Recent findings research has highlighted significant pathogenesis via gut-brain axis. However, precise mechanisms by which and its microbial metabolites influence brain function are not clearly understood. Various factors, such as diet, drugs, lifestyle, stress, infections can provoke imbalance homeostasis, known dysbiosis. This dysbiosis impacts intestinal blood-brain barrier permeability, elevating pro-inflammatory cytokines contributing neurodegeneration. Moreover, generates neurotransmitters, amyloids, neurotoxins, metabolites, may play a systemic inflammation disruption physiological barriers. Summary In past decade, advancements analysis technologies bioinformatics have significantly enhanced our disease. plays pivotal regulatory progression disease, closely interacts with pathogenesis, encompassing inflammation, amyloidosis, neurodegeneration, tauopathy, co-pathologies.
Язык: Английский
Процитировано
0
Journal of Alzheimer s Disease, Год журнала: 2025, Номер unknown
Опубликована: Март 17, 2025
Background The roles of complement 1q (C1q) and Apolipoprotein E (ApoE) in driving Alzheimer's disease (AD) progression might be explained by their associations with neuroinflammation AD pathology which were previously reported. Objective We examined the cerebrospinal fluid (CSF) C1q ApoE CSF neuroinflammatory biomarkers core biomarkers, as well explored whether mediated these biomarkers. Methods Here, we analyzed proteomics data from Disease Neuroimaging Initiative (ADNI) using two different ADNI datasets—SomaScan (n = 579)and multiple reaction monitoring (MRM[n 207]). Linear regression analyses conducted to explore association C1q. mediation model structural equation (SEM) Results Multiple linear showed that was positively associated total participants continuum participants. Mediation indicated T-tau, P-tau, sTREM2 GFAP (mediation proportions range 15.06 44.64%; all p values < 0.05) but not amyloid-β progranulin (PGRN). SEM yielded similar results. Conclusions Our findings suggest is linked ApoE, it mediates sTREM2, GFAP, indicating involved progression.
Язык: Английский
Процитировано
0
Ageing Research Reviews, Год журнала: 2025, Номер unknown, С. 102732 - 102732
Опубликована: Март 1, 2025
Язык: Английский
Процитировано
0
Neurotherapeutics, Год журнала: 2025, Номер unknown, С. e00586 - e00586
Опубликована: Апрель 1, 2025
Язык: Английский
Процитировано
0
Journal of Alzheimer s Disease, Год журнала: 2024, Номер 102(2), С. 314 - 316
Опубликована: Ноя. 1, 2024
This commentary offers a detailed examination of newly published paper on the effects small molecule decoys amyloid-β (Aβ) aggregation microglial activation. It was discovered that NSC16224 decoy peptide inhibited proinflammatory cytokines TNFα and IL6 release from microglia in response to Aβ
Язык: Английский
Процитировано
0
Neuropharmacology, Год журнала: 2024, Номер unknown, С. 110241 - 110241
Опубликована: Ноя. 1, 2024
Язык: Английский
Процитировано
0