Neurodegenerative disorders such as Alzheimer's disease (AD) and Parkinson's disease (PD) are becoming more frequent as the age increases. Contemporary therapies provide symptom resolution instead of targeting underlying pathological pathways. Consequently, there is considerable heterogeneity in response to treatment. Research has elucidated multiple potential of pathophysiological mechanisms contributing to neurodegenerative conditions, among which oxidative stress pathways appear to be suitable drug targets. The oxidative stress pathway has given rise to numerous novel pharmacological therapies that may provide a new avenue for neurodegenerative diseases. For example, SKQ (plastoquinone), MitoVitE, vitamin E, SOD mimic, MitoTEMPO (SOD mimetic), and bioactive molecules like curcumin and vitamin C have indeed been examined. To better understand how oxidative stress contributes to neurodegenerative diseases (such as Alzheimer's and Parkinson's), we analyzed the medicinal qualities of medicines that target markers in the cellular oxidative pathways. The specific pathway by which mitochondrial dysfunction causes neurodegeneration will require more investigation. An animal study should be carried out on medications that tackle cellular redox mechanisms but are not currently licensed for use in the management of neurodegenerative conditions.
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http://dx.doi.org/10.1155/2022/7934442 | DOI Listing |
BMC Endocr Disord
January 2025
School of Public Health, Anhui Medical University, No. 81 Meishan Road, Hefei, Anhui, 230032, China.
Background: As the prevalence of metabolic syndrome (MetS) rises among older adults, the associated risks of cardiovascular diseases and diabetes significantly increase, and it is closely linked to various metabolic processes in the body. Dysregulation of tryptophan (TRP) metabolism, particularly alterations in the kynurenine (KYN) and serotonin pathways, has been linked to the onset of chronic inflammation, oxidative stress, and insulin resistance, key contributors to the development of MetS. We aim to investigate the relationship between the TRP metabolites and the risk of MetS in older adults.
View Article and Find Full Text PDFAn experiment was conducted for 60 days in a 500L capacity FRP tank containing inland ground saline water (fortified to a level of 50% potassium) with one control (sediment) and three treatments; T1(Paddy Straw Biochar (PSB) in sediment), T2 (Banana Peduncle Biochar (BPB) in sediment), and T3 (PSB + BPB in sediment). Biochar (100 g) was amended with sediment (25 kg) at 9 tons/ha. Shrimps of average weight 5 ± 0.
View Article and Find Full Text PDFSci Rep
January 2025
Environmental Toxicology & Bioremediation Laboratory (ETBL), Department of Zoology, University of Lucknow, Lucknow, 226007, India.
Herbicide paraquat dichloride, a potent redox agent found its way to natural water bodies and influences their health; however, its impact on the reproductive health of fish is potentially less studied and requires clear investigation. This study was conducted to elucidate its effect on the gonadal health of female fish, Channa punctatus over 60 days. The 96-h LC of test herbicide was calculated as 0.
View Article and Find Full Text PDFNature
January 2025
Institut für Biochemie, Albert-Ludwigs-Universität Freiburg, Freiburg im Breisgau, Germany.
The oxygen-sensitive molybdenum-dependent nitrogenase of Azotobacter vinelandii is protected from oxidative damage by a reversible 'switch-off' mechanism. It forms a complex with a small ferredoxin, FeSII (ref. ) or the 'Shethna protein II', which acts as an O sensor and associates with the two component proteins of nitrogenase when its [2Fe:2S] cluster becomes oxidized.
View Article and Find Full Text PDFNat Commun
January 2025
Tulane Center for Biomedical Informatics and Genomics, Deming Department of Medicine, School of Medicine, Tulane University, New Orleans, LA, 70112, USA.
Aging increases the risk for Alzheimer's disease (AD), driving pathological changes like amyloid-β (Aβ) buildup, inflammation, and oxidative stress, especially in the prefrontal cortex (PFC). We present the first subcellular-resolution spatial transcriptome atlas of the human prefrontal cortex (PFC), generated with Stereo-seq from six male AD cases at varying neuropathological stages and six age-matched male controls. Our analyses revealed distinct transcriptional alterations across PFC layers, highlighted disruptions in laminar structure, and exposed AD-related shifts in layer-to-layer and cell-cell interactions.
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