Persistent diazinon induced neurotoxicity: The effect on inhibitory avoidance memory performance, amyloid precursor proteins, and TNF-α levels in the prefrontal cortex of rats DOI Creative Commons
Salva Afshari, Mehdi Sarailoo, Vahid Asghariazar

et al.

Human & Experimental Toxicology, Journal Year: 2024, Volume and Issue: 43

Published: Jan. 1, 2024

Introduction Organophosphate pesticides (Ops) like diazinon (DZN) have well-known neurotoxic effects and low-level chronic exposure has been linked to detrimental neurobehavioral impairments memory deficits. However, it’s not entirely clear how DZN-induced biological changes, particularly in the prefrontal cortex (PFC) contribute these effects. The purpose of this study is investigate impact DZN on inhibitory avoidance (IA) function, amyloid precursor expression (APP), proinflammatory tumor necrosis factor-α (TNF-α) levels rat cortex. Materials Methods Rats were divided into 4 groups recived 2 mg/kg for 5-days or 12-weeks two control same volume vehicle. IA was assesed using shuttle box apparatus. sacrificed PFC removed. Real-time PCR Western blotting used messure TNF-α, protein precursors gene levels. Results Our findings indicated that caused body weight loss a notable decline performance memory. Additionally, increased APP APLP2 PFC, while decreased Furthermore, gens PFC. TNF-α as result DZN, but dropped normal after administration, observation significant. Conclusion Taken together, low doses leads disturbances also alternations beta can be related risk Alzheimer’s disease.

Language: Английский

Blood-Based Biomarkers of Neuroinflammation in Alzheimer’s Disease: A Central Role for Periphery? DOI Creative Commons

Federica Angiulli,

Elisa Conti, C Zoia

et al.

Diagnostics, Journal Year: 2021, Volume and Issue: 11(9), P. 1525 - 1525

Published: Aug. 24, 2021

Neuroinflammation represents a central feature in the development of Alzheimer’s disease (AD). The resident innate immune cells brain are principal players neuroinflammation, and their activation leads to defensive response aimed at promoting β-amyloid (Aβ) clearance. However, it is now widely accepted that peripheral system—by virtue dysfunctional blood–brain barrier (BBB)—is involved pathogenesis progression AD; microglial astrocytic release chemokines able recruit into nervous system (CNS); same time, cytokines released by cross BBB act upon glial cells, modifying phenotype. To successfully fight this neurodegenerative disorder, accurate sensitive biomarkers required be used for implementing an early diagnosis, monitoring treatment effectiveness. Interestingly, as result bidirectional communication between periphery, blood compartment ends up reflecting several pathological changes occurring AD can represent accessible source such biomarkers. In review, we provide overview on some most promising discussing pathogenic role AD.

Language: Английский

Citations

39

Thioredoxin-interacting protein (TXNIP) as a target for Alzheimer’s disease: flavonoids and phenols DOI
Meng Zhang, Guanhua Hu, Nan Shao

et al.

Inflammopharmacology, Journal Year: 2021, Volume and Issue: 29(5), P. 1317 - 1329

Published: Aug. 4, 2021

Language: Английский

Citations

35

Immune system-wide Mendelian randomization and triangulation analyses support autoimmunity as a modifiable component in dementia-causing diseases DOI Creative Commons
Joni V. Lindbohm, Nina Mars, Pyry N. Sipilä

et al.

Nature Aging, Journal Year: 2022, Volume and Issue: 2(10), P. 956 - 972

Published: Oct. 14, 2022

Immune system and blood-brain barrier dysfunction are implicated in the development of Alzheimer's other dementia-causing diseases, but their causal role remains unknown. We performed Mendelian randomization for 1,827 immune system- barrier-related biomarkers identified 127 potential risk factors diseases. Pathway analyses linked these to amyloid-β, tau α-synuclein pathways autoimmunity-related processes. A phenome-wide analysis using randomization-based polygenic score FinnGen study (n = 339,233) indicated shared genetic background dementias autoimmune This association was further supported by human leukocyte antigen analyses. In inverse-probability-weighted that simulate randomized controlled drug trials observational data, anti-inflammatory methotrexate treatment reduced incidence disease high-risk individuals (hazard ratio compared with no treatment, 0.64, 95% confidence interval 0.49-0.88, P 0.005). These converging results from different lines research suggest autoimmunity is a modifiable component

Language: Английский

Citations

25

Lantana camara leaf extract ameliorates memory deficit and the neuroinflammation associated with scopolamine-induced Alzheimer’s-like cognitive impairment in zebrafish and mice DOI Creative Commons
Veronica Amoah, Paul Atawuchugi, Jibira Yakubu

et al.

Pharmaceutical Biology, Journal Year: 2023, Volume and Issue: 61(1), P. 825 - 838

Published: May 22, 2023

Lantana camara Linn. (Verbenaceae) is used for improving memory in certain African societies.This study investigated the effect of prophylactic treatment with hydroethanolic leaf extract (LCE) on short-term deficit and neuroinflammation induced scopolamine zebrafish mice.Zebrafish (AB strain) mice (ICR) were given donepezil (0.65 mg/kg, oral) LCE (10, 30, 100 7, 10 days, respectively, before induction cognitive impairment immersion (200 µM) intraperitoneal injection (2 mg/kg), respectively. Spatial was assessed using both Y- T-mazes, whereas Y-maze mice. Mice hippocampal cortical tissues analyzed mRNA expression proinflammatory genes (IL-1β, IL-6, TNF-α, COX-2) qRT-PCR.In Y-maze, (10 mg/kg) increased time spent novel arm by 55.89 ± 5.70%, 68.21 2.75%, but not at 30 mg/kg. In T-maze, there an increase food-containing (44.23 2.13) mg/kg (52.30 1.94). mouse spontaneous alternation 52.89 4.98% only inhibited gene expression, highest inhibitory IL-6 hippocampus (83.27 2.49%; cortex (98.74 0.11%; mg/kg).LCE ameliorated scopolamine-induced AD

Language: Английский

Citations

14

Persistent diazinon induced neurotoxicity: The effect on inhibitory avoidance memory performance, amyloid precursor proteins, and TNF-α levels in the prefrontal cortex of rats DOI Creative Commons
Salva Afshari, Mehdi Sarailoo, Vahid Asghariazar

et al.

Human & Experimental Toxicology, Journal Year: 2024, Volume and Issue: 43

Published: Jan. 1, 2024

Introduction Organophosphate pesticides (Ops) like diazinon (DZN) have well-known neurotoxic effects and low-level chronic exposure has been linked to detrimental neurobehavioral impairments memory deficits. However, it’s not entirely clear how DZN-induced biological changes, particularly in the prefrontal cortex (PFC) contribute these effects. The purpose of this study is investigate impact DZN on inhibitory avoidance (IA) function, amyloid precursor expression (APP), proinflammatory tumor necrosis factor-α (TNF-α) levels rat cortex. Materials Methods Rats were divided into 4 groups recived 2 mg/kg for 5-days or 12-weeks two control same volume vehicle. IA was assesed using shuttle box apparatus. sacrificed PFC removed. Real-time PCR Western blotting used messure TNF-α, protein precursors gene levels. Results Our findings indicated that caused body weight loss a notable decline performance memory. Additionally, increased APP APLP2 PFC, while decreased Furthermore, gens PFC. TNF-α as result DZN, but dropped normal after administration, observation significant. Conclusion Taken together, low doses leads disturbances also alternations beta can be related risk Alzheimer’s disease.

Language: Английский

Citations

5