Current Progress on Postoperative Cognitive Dysfunction: An Update DOI Creative Commons
Jing Sun, Xiaohong Du, Yong Chen

et al.

Journal of Integrative Neuroscience, Journal Year: 2024, Volume and Issue: 23(12)

Published: Dec. 24, 2024

Postoperative cognitive dysfunction (POCD) represents a significant clinical concern, particularly among elderly surgical patients. It is characterized by decline in performance, affecting memory, attention, coordination, orientation, verbal fluency, and executive function. This abilities leads to longer hospital stays increased mortality. review provides comprehensive overview of the current progress understanding relevant pathogenic factors, possible mechanisms, diagnosing, prevention treatment POCD, as well suggesting future research directions. discusses neuronal damage, susceptible genes, central cholinergic system, nervous system (CNS) inflammation, stress response glucocorticoids, oxidative development aiming uncover pathological mechanism develop effective strategies for POCD.

Language: Английский

Aging device: tau protein transposes the telomerase fragment into promoter/enhancer to promote gene copy number decrement regulation DOI Creative Commons
Wenzhong Liu,

Li hualan

Published: Aug. 2, 2024

The reasons for the significant impact of abnormal tau protein phosphorylation and aggregation on Alzheimer's disease are still unknown. This study used bioinformatics methods, including domain search tools, to investigate pathogenic mechanism in neurodegenerative diseases. reveals that possesses domains linked Aging Device. These include pyruvate kinase, phosphatase, telomere binding, transposition, HNH cas9, replicon helicase, DNA polymerase, nuclease, transcription factors-like, promoter binding (TATA-box), enhancer (Homeobox, MADS-box, HMG box), mitochondrial localization mtDNA polymerase. It implies protein's kinase supplies ATP energy its Device function. Cas9 , reverse transcriptase, transposase cut sequence between "TAA" from then transcript guide RNA sequence. factor slides specific region. excises intron region complementary RAN nuclease splice or add fragment We thought transposes fragments promoter/enhancer might mess up polymerase II, which would help Device's telomere-guided gene (DNA nucleus mitochondrial) copy number decrement regulation system work better. can us understand how stress injuries, like low blood sugar oxygen levels, cause clump together phosphorylate, turns off a way doesn't make sense. Thus, anomalous aging devices, such as protein, may be associated with diseases Alzheimer disease, amyotrophic lateral sclerosis.

Language: Английский

Citations

1

Inhibition of Protease-Activated Receptor-2 Activation in Parkinson’s Disease Using 1-Piperidin Propionic Acid DOI Creative Commons
Santina Quarta, Michele Sandre, Mariagrazia Ruvoletto

et al.

Biomedicines, Journal Year: 2024, Volume and Issue: 12(7), P. 1623 - 1623

Published: July 22, 2024

In Parkinson's disease, neuroinflammation is a double-edged sword; when inflammation occurs it can have harmful effects, despite its important role in battling infections and healing tissue. Once triggered by microglia, astrocytes acquire reactive state shift from supporting the survival of neurons to causing their destruction. Activated microglia Proteinase-activated receptor-2 (PAR2) are key points regulation neuroinflammation. 1-Piperidin Propionic Acid (1-PPA) has been recently described as novel inhibitor PAR2. The aim our study was evaluate effect 1-PPA microglial activation disease. Protein aggregates PAR2 expression were analyzed using Thioflavin S assay immunofluorescence cultured human fibroblasts patients, treated or untreated with 1-PPA. A significant decrease amyloid observed after treatment all patients. parallel expression, which higher sporadic also both at transcriptional protein level. addition, mouse LPS-activated inflammatory profile significantly downregulated treatment, remarkable IL-1β, IL-6, TNF-α, together decreased conclusion, determines reduction neuroglia formation, suggesting that pharmacological inhibition could be proposed strategy control

Language: Английский

Citations

0

Human Target Proteins for Benzo(a)pyrene and Acetaminophen (and Its Metabolites): Insights from Inverse Molecular Docking and Molecular Dynamics Simulations DOI Creative Commons
Y. P., Nérlis Pájaro-Castro,

Nadia Coronado‐Posada

et al.

Scientia Pharmaceutica, Journal Year: 2024, Volume and Issue: 92(4), P. 55 - 55

Published: Oct. 8, 2024

Acetaminophen (APAP) is a widely used analgesic and antipyretic, whereas benzo(a)pyrene (B[a]P) carcinogen with significant global health risks due to environmental exposure. While APAP generally safe at therapeutic doses, co-exposure B[a]P can exacerbate its toxicity. This study aimed identify potential human target proteins for through inverse molecular docking dynamics simulations. We performed B[a]P, APAP, three metabolites against 689 involved in various biological processes. Five were selected based on high affinity their involvement multiple pathways. Molecular simulations revealed that primarily interacted via hydrophobic π-stacking interactions like LXR-β, HSP90α, HSP90β, AKT1, while AM404 formed hydrogen bonds interactions. The confirmed the complexes had conformational stability, except protein AKT1. These results provide insights into impacts of functions implications understanding toxic effects combined

Language: Английский

Citations

0

Current Progress on Postoperative Cognitive Dysfunction: An Update DOI Creative Commons
Jing Sun, Xiaohong Du, Yong Chen

et al.

Journal of Integrative Neuroscience, Journal Year: 2024, Volume and Issue: 23(12)

Published: Dec. 24, 2024

Postoperative cognitive dysfunction (POCD) represents a significant clinical concern, particularly among elderly surgical patients. It is characterized by decline in performance, affecting memory, attention, coordination, orientation, verbal fluency, and executive function. This abilities leads to longer hospital stays increased mortality. review provides comprehensive overview of the current progress understanding relevant pathogenic factors, possible mechanisms, diagnosing, prevention treatment POCD, as well suggesting future research directions. discusses neuronal damage, susceptible genes, central cholinergic system, nervous system (CNS) inflammation, stress response glucocorticoids, oxidative development aiming uncover pathological mechanism develop effective strategies for POCD.

Language: Английский

Citations

0