Cerebral edema and cognitive dysfunction: pathophysiological interconnections in diabetic ketoacidosis in childhood DOI Open Access
Yuri V. Bykov

Pediatrician (St Petersburg), Journal Year: 2024, Volume and Issue: 15(4), P. 63 - 71

Published: Dec. 30, 2024

Diabetic ketoacidosis is one of the most common complications in children suffering from diabetes mellitus, a complication that may cause cerebral edema. After diabetic episode, some develop cognitive impairment, which could be linked to subclinical or clinical grade An analysis scientific literature has shown pathophysiological mechanisms development dysfunction with ketoacidosis-associated edema have not been fully elucidated. The key pathogenetic hypotheses under consideration include hypoxia, hypoperfusion and reperfusion, release vasoactive substances induction inflammation, acute hyperglycemia oxidative stress. Hypoxia leads hypoxic-ischaemic injury brain, affecting, among others, areas responsible for memory formation. Cerebral reperfusion trigger mitochondrial stress, worsens impairment patients Release inflammation impair functioning blood-brain barrier lead vasospasm. Acute hypoglycemia triggers brain tissue acidosis accumulation lactate glutamate, aggravating dysfunction. Oxidative stress causes neuronal damage, exacerbating manifestations described here setting either as individual collectively through synergistic effect. Further research needed expand knowledge interconnections between after episode.

Language: Английский

Understanding mechanisms of antioxidant action in health and disease DOI
Barry Halliwell

Nature Reviews Molecular Cell Biology, Journal Year: 2023, Volume and Issue: 25(1), P. 13 - 33

Published: Sept. 15, 2023

Language: Английский

Citations

237

Oxidative damage in neurodegeneration: roles in the pathogenesis and progression of Alzheimer disease DOI
Marzia Perluigi, Fabio Di Domenico, D. Allan Butterfield

et al.

Physiological Reviews, Journal Year: 2023, Volume and Issue: 104(1), P. 103 - 197

Published: Oct. 16, 2023

Alzheimer disease (AD) is associated with multiple etiologies and pathological mechanisms, among which oxidative stress (OS) appears as a major determinant. Intriguingly, OS arises in various pathways regulating brain functions, it seems to link different hypotheses mechanisms of AD neuropathology high fidelity. The particularly vulnerable damage, mainly because its unique lipid composition, resulting an amplified cascade redox reactions that target several cellular components/functions ultimately leading neurodegeneration. present review highlights the “OS hypothesis AD,” including amyloid beta-peptide-associated role protein oxidation unraveled by proteomics, antioxidant strategies have been investigated modulate progression AD. Collected studies from our groups others contributed unraveling close relationships between perturbation homeostasis elucidating redox-regulated events potentially involved both pathogenesis However, complexity requires in-depth understanding intracellular affecting relevant for functions. This crucial developing pharmacological targeting OS-mediated toxicity may contribute slow well improve quality life persons this severe dementing disorder.

Language: Английский

Citations

77

Mechanisms of autophagy–lysosome dysfunction in neurodegenerative diseases DOI
Ralph A. Nixon, David C. Rubinsztein

Nature Reviews Molecular Cell Biology, Journal Year: 2024, Volume and Issue: 25(11), P. 926 - 946

Published: Aug. 6, 2024

Language: Английский

Citations

54

Autophagy–lysosomal-associated neuronal death in neurodegenerative disease DOI
Ralph A. Nixon

Acta Neuropathologica, Journal Year: 2024, Volume and Issue: 148(1)

Published: Sept. 11, 2024

Language: Английский

Citations

9

Development of chitosan lipid nanoparticles to alleviate the pharmacological activity of piperine in the management of cognitive deficit in diabetic rats DOI Creative Commons
Asmaa Badawy Darwish, Amira Mohamed Mohsen, Shaimaa ElShebiney

et al.

Scientific Reports, Journal Year: 2024, Volume and Issue: 14(1)

Published: April 8, 2024

The aim of the present study was to prepare and evaluate Piperine (PP) loaded chitosan lipid nanoparticles (PP-CLNPs) its biological activity alone or in combination with antidiabetic drug Metformin (MET) management cognitive deficit diabetic rats. successfully on CLNPs prepared using chitosan, stearic acid, Tween 80 Tripolyphosphate (TPP) at different concentrations. developed exhibited high entrapment efficiency that ranged from 85.12 97.41%, a particle size range 59.56-414 nm negatively charged zeta potential values (- 20.1 - 43.9 mV). In vitro release revealed enhanced PP compared free suspensions for up 24 h. vivo studies treatment optimized PP-CLNPs formulation (F2) exerted enhancing effect ameliorated oxidative stress associated diabetes. acted as an effective bio-enhancer which increased potency metformin protecting brain tissue diabetes-induced neuroinflammation memory deterioration. These results suggested could be promising delivery system encapsulating thus can used adjuvant therapy high-risk impairment conditions.

Language: Английский

Citations

8

Vicious cycle of oxidative stress and neuroinflammation in pathophysiology of chronic vascular encephalopathy DOI Creative Commons
Tetiana R. Dmytriv, Khrystyna Duve, Kenneth B. Storey

et al.

Frontiers in Physiology, Journal Year: 2024, Volume and Issue: 15

Published: Aug. 5, 2024

Chronic vascular encephalopathy (CVE) is a frequent cause of mild cognitive impairment and dementia, which significantly worsens the quality life, especially in elderly population. CVE result chronic cerebral hypoperfusion, characterized by prolonged limited blood flow to brain. This causes insufficient oxygenation brain leading hypoxia. The latter can trigger series events associated with development oxidative/reductive stresses neuroinflammation. Addressing gap knowledge regarding oxidative reductive disorders neuroinflammation give start new directions research context CVE. In this review, we consider hypoxia-induced molecular challenges involved pathophysiology CVE, focusing on stress neuroinflammation, are combined vicious cycle neurodegeneration. We also briefly describe therapeutic approaches treatment outline prospects for use sulforaphane, an isothiocyanate common cruciferous plants, vitamin D break alleviate impairments characteristic patients

Language: Английский

Citations

8

NOX-induced oxidative stress is a primary trigger of major neurodegenerative disorders DOI Creative Commons
Yuri Zilberter, Dennis R. Tabuena, Misha Zilberter

et al.

Progress in Neurobiology, Journal Year: 2023, Volume and Issue: 231, P. 102539 - 102539

Published: Oct. 12, 2023

Neurodegenerative diseases (NDDs) causing cognitive impairment and dementia are difficult to treat due the lack of understanding primary initiating factors. Meanwhile, major sporadic NDDs share many risk factors exhibit similar pathologies in their early stages, indicating existence common initiation pathways. Glucose hypometabolism associated with oxidative stress is one such primary, shared pathology, a likely cause detrimental disease-associated cascades; targeting this pathology may therefore be an effective preventative strategy for most NDDs. However, its exact trigger remain unclear. Recent research suggests that caused by NADPH oxidase (NOX) activation mechanism among could prove long-sought ubiquitous NDD trigger. We focus on two - Alzheimer's disease (AD) Parkinson's (PD), as well acquired epilepsy which increasingly recognized comorbidity also discuss available data suggesting relevance proposed mechanisms other delve into commonalities these neuroinflammation NOX involvement identify potential therapeutic targets gain deeper underlying causes

Language: Английский

Citations

13

MicroRNAs signatures as potential molecular markers in mild cognitive impairment: a meta-analysis DOI Creative Commons

Natalia Vargas-Rondón,

Yeimy González‐Giraldo, Angela Garcia

et al.

Frontiers in Aging Neuroscience, Journal Year: 2025, Volume and Issue: 16

Published: Jan. 15, 2025

Mild cognitive impairment (MCI) is characterized by a decline in functioning without significant interference daily activities. Its high heterogeneity and elevated conversion rate to dementia pose challenges for accurate diagnosis monitoring, highlighting the urgent need identify methodologies focused on early detection intervention of MCI. Due their biological characteristics, microRNAs (miRNAs) are potential candidates as non-invasive molecular markers identification assessment MCI progression. Therefore, this study, we conducted meta-analysis miRNAs commonly deregulated MCI, focusing expression profiles plasma, serum, extracellular vesicle samples. Our analysis identified eight upregulated miRNAs, including hsa-miR-149-3p, four downregulated such Let-7f-5p. Notably, hsa-miR-149-3p emerged central node interaction networks, suggesting its crucial role regulating cellular processes relevant Additionally, pathway revealed enrichment associated with transcriptional regulation neurodegeneration. results underscore circulating open possibility new that enable more monitoring disease Validating Let-7f-5p, along identifying functional specific context essential establish relevance. This work contributes understanding miRNA profile mild using easily accessible samples, which could be useful development various strategies aimed at preventing or delaying individuals risk developing dementia, Alzheimer's disease.

Language: Английский

Citations

0

Lateral hypothalamic area high-frequency deep brain stimulation rescues memory decline in aged rat: behavioral, molecular, and electrophysiological study DOI Creative Commons
Abdelaziz M. Hussein,

Ahmed Abouelnaga,

Walaa Obydah

et al.

Pflügers Archiv - European Journal of Physiology, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 21, 2025

Language: Английский

Citations

0

Serum and Cerebrospinal Fluid Malondialdehyde Levels in Patients with Mild Cognitive Impairment DOI Creative Commons
Stavroula Ioannidou, Argyrios Ginoudis, Kali Makedou

et al.

Journal of Xenobiotics, Journal Year: 2025, Volume and Issue: 15(2), P. 50 - 50

Published: March 30, 2025

Mild cognitive impairment (MCI) is recognized as an intermediate stage between normal aging and dementia. Oxidative stress implicated in the pathophysiology of neurodegenerative diseases, playing a crucial role. This study aimed to investigate differences malondialdehyde (MDA) levels serum cerebrospinal fluid (CSF) patients with MCI compared FDA-approved biomarkers, based on age, sex, education level. Participants aged 55–90 years old were categorized into three groups especially CSF Aβ42/Aβ40 ratio clinical screening assessments: 30 (A+) abnormal ratios (Group A), (A−) B), healthy participants C). The measurements biomarkers performed using automated immunochemical method (Fujirebio, Inc.), while MDA determination was competitive inhibition enzyme immunoassay technique (ELK Biotechnology Co., Ltd.). Our results showed that mean values significantly lower group C than A (83 ng/mL vs. 130 ng/mL, p = 0.024) B 142 0.011), respectively. Differences presented These findings suggest lipid peroxidation, indicated by MDA, could serve potential biomarker for early recognition MCI.

Language: Английский

Citations

0