Drug Discovery Today, Год журнала: 2025, Номер unknown, С. 104375 - 104375
Опубликована: Май 1, 2025
Язык: Английский
CNS Neuroscience & Therapeutics, Год журнала: 2023, Номер 30(3)
Опубликована: Окт. 30, 2023
Abstract Background Gemfibrozil (Gem) is a drug that has been shown to activate PPAR‐α, nuclear receptor plays key role in regulating lipid metabolism. Gem used lower the levels of triglycerides and reduce risk coronary heart disease patients. Experimental studies vitro vivo have can prevent or slow progression neurological disorders (NDs), including cerebral ischemia (CI), Alzheimer's (AD), Parkinson's (PD), multiple sclerosis (MS). Neuroinflammation known play significant these disorders. Method The literature review for this study was conducted by searching Scopus, Science Direct, PubMed, Google Scholar databases. Result results show neuroprotective effects through several cellular molecular mechanisms such as: (1) ability upregulate pro‐survival factors (PGC‐1α TFAM), promoting survival function mitochondria brain, (2) strongly inhibits activation NF‐κB, AP‐1, C/EBPβ cytokine‐stimulated astroglial cells, which are increase expression iNOS production NO response proinflammatory cytokines, (3) protects dopamine neurons MPTP mouse model PD increasing PPARα, turn stimulates GDNF astrocytes, (4) reduces amyloid plaque pathology, activity glial improves memory, (5) increases myelin genes (MBP CNPase) via PPAR‐β, (6) hippocampal BDNF counteract depression. Conclusion According study, investigated its potential therapeutic effect NDs. Further research needed fully understand
Язык: Английский
Процитировано
17
Molecular Neurobiology, Год журнала: 2024, Номер 61(8), С. 5826 - 5840
Опубликована: Янв. 18, 2024
Язык: Английский
Процитировано
6
Frontiers in Aging Neuroscience, Год журнала: 2024, Номер 16
Опубликована: Фев. 28, 2024
Sensorineural hearing loss (SNHL) is a category of that often leads to difficulty in understanding speech and other sounds. Auditory system dysfunction, including deafness auditory trauma, results cognitive deficits via neuroplasticity. Cognitive impairment (CI) refers an abnormality the brain’s higher intellectual processes related learning, memory, thinking judgment can lead severe learning memory deficits. Studies have established strong correlation between SNHL CI, but it remains unclear how contributes CI. The purpose this article describe three hypotheses regarding relationship, mainstream load hypothesis, co-morbidity sensory deprivation as well latest research progress each hypothesis.
Язык: Английский
Процитировано
6
Pharmaceutics, Год журнала: 2024, Номер 16(6), С. 708 - 708
Опубликована: Май 24, 2024
Neurodegenerative diseases (NDs) are a set of progressive, chronic, and incurable characterized by the gradual loss neurons, culminating in decline cognitive and/or motor functions. Alzheimer’s disease (AD) Parkinson’s (PD) most common NDs represent an enormous burden both terms human suffering economic cost. The available therapies for AD PD only provide symptomatic palliative relief limited period unable to modify diseases’ progression. Over last decades, research efforts have been focused on developing new pharmacological treatments these NDs. However, date, no breakthrough treatment has discovered. Hence, development disease-modifying drugs able halt or reverse progression remains unmet clinical need. This review summarizes major hallmarks treatment. It also sheds light potential directions that can be pursued develop new, treat PD, describing as representative examples some advances drug candidates targeting oxidative stress adenosine A2A receptors.
Язык: Английский
Процитировано
6
Archives of Oral Biology, Год журнала: 2023, Номер 147, С. 105632 - 105632
Опубликована: Янв. 28, 2023
Язык: Английский
Процитировано
12
Frontiers in Molecular Neuroscience, Год журнала: 2023, Номер 16
Опубликована: Май 12, 2023
Recent advances highlight that inflammation is critical to Alzheimer Disease (AD) pathogenesis. Indeed, several diseases characterized by are considered risk factors for AD, such as type 2 diabetes, obesity, hypertension, and traumatic brain injury. Moreover, allelic variations in genes involved the inflammatory cascade AD. AD also mitochondrial dysfunction, which affects energy homeostasis of brain. The role dysfunction has been mostly neuronal cells. However, recent data demonstrating occurs cells, promoting secretion pro-inflammatory cytokines, turn induce neurodegeneration. In this review, we summarize finding supporting hypothesis inflammatory-amyloid describe demonstrate link between altered cascade. We focus summarizing Drp1, fission, showing Drp1 activation leads NLRP3 inflammasome, cascade, aggravates Amyloid beta (Ab) deposition tau-induced neurodegeneration, relevance pathway an early event
Язык: Английский
Процитировано
12
Immunological Reviews, Год журнала: 2023, Номер 322(1), С. 259 - 282
Опубликована: Дек. 25, 2023
Summary From studies of individual families to global collaborative efforts, the NLRP3 inflammasome is now recognized be a key regulator innate immunity. Activated by panoply pathogen‐associated and endogenous triggers, serves as an intracellular sensor that drives carefully coordinated assembly inflammasome, downstream inflammation mediated IL‐1 IL‐18. Initially discovered cause autoinflammatory spectrum cryopyrin‐associated periodic syndrome (CAPS), also known play role in more common diseases including cardiovascular disease, gout, liver disease. We have seen cohesion results from clinical CAPS patients, ex vivo human cells murine cells, models leading our understanding pathways, cytokine secretion, cell death pathways has solidified autoinflammation pathogenesis Recent advances structure provided ways for us visualize normal mutant protein function pharmacologic inhibition. The subsequent development targeted therapies successfully used treatment patients with completes bench bedside translational loop which defined study this unique protein.
Язык: Английский
Процитировано
11
British Journal of Pharmacology, Год журнала: 2023, Номер 181(6), С. 840 - 878
Опубликована: Сен. 14, 2023
Adipose tissue has recently been recognized as an important endocrine organ that plays a crucial role in energy metabolism and the immune response many metabolic tissues. With this regard, emerging evidence indicates crosstalk exists between adipose brain. However, contribution of to development age-related diseases, including Alzheimer's disease, remains poorly defined. New studies suggest modulates brain function through range endogenous biologically active factors known adipokines, which can cross blood-brain barrier reach target areas or regulate barrier. In review, we discuss effects several adipokines on physiology barrier, their disease therapeutic potential. LINKED ARTICLES: This article is part themed issue From Disease Vascular Dementia: Different Roads Leading Cognitive Decline. To view other articles section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v181.6/issuetoc.
Язык: Английский
Процитировано
10
medRxiv (Cold Spring Harbor Laboratory), Год журнала: 2025, Номер unknown
Опубликована: Янв. 10, 2025
Abstract Background Alzheimer’s disease (AD) is the most common neurodegenerative disorder, NLRP3 inflammasome has been shown to play a pivotal role in pathogenesis of AD, and with increasing attention its involvement AD. Therefore, we applied bibliometric methods describe current research status This study aims analyze trends hotspots this field from 2013 2024, providing valuable insights for AD research. Methods We have selected on Web Science Core Collection, time range January 1, 2013, November 30, exported all publications plain text format. Visualization analysis was performed using CiteSpace 6.4.R1, VOSviewer 1.6.20, Scimago Graphica 1.0.46. Results A total 759 related were included study. The number annual showed general upward trend. top three countries terms publication volume China, United States, Italy. University Manchester institution highest publications. author Michael Heneka, while cited Eicke Latz. International Journal Molecular Sciences published articles also frequently journal. keywords disease, inflammasome, neuroinflammation, Aβ, microglia. Conclusion primary focus pathology, potential as therapeutic target, strategies modulate neuroinflammation through targeting inflammasome. Future should further investigate interactions between other molecular pathways, assess clinical potential, provide new early diagnosis treatment
Язык: Английский
Процитировано
0
NeuroMolecular Medicine, Год журнала: 2025, Номер 27(1)
Опубликована: Март 7, 2025
Язык: Английский
Процитировано
0