The effects of intra-dorsal hippocampus infusion of pregnenolone sulfate on memory function and hippocampal BDNF mRNA expression of biliary cirrhosis-induced memory impairment in rats

Dastgheib, Mona; Dehpour, Ahmad Reza; Heidari, Mansour; Moezi, Leila

doi:10.1016/j.neuroscience.2015.08.018

Cited by 18 publications

(6 citation statements)

References 62 publications

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“…BDNF supports synaptic plasticity and is critically involved in memory processing. Previous reports have shown decreased hippocampal BDNF mRNA in adult BDL rats 22 and decreased prefrontal cortex BDNF mRNA in young BDL rats 13 . Here, we showed a decrease in BDNF expression in BDL rats’ dorsal hippocampus that was prevented by melatonin, suggesting a role of BDNF in cognition deficits in BDL rats.…”

Section: Discussionmentioning

confidence: 75%

Melatonin prevented spatial deficits and increases in brain asymmetric dimethylarginine in young bile duct ligation rats

et al. 2018

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Bile duct ligation (BDL) in young rats can cause impaired liver function and cognition deficits. Nitric oxide is implicated in hepatic encephalopathy and is also involved in cognition. In this study, we examined the role of brain asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase inhibitor, in young BDL rats with spatial deficits. Young male Sprague-Dawley rats aged 17 days were assigned to four groups: laparotomy (SHAM), laparotomy plus 5 mg melatonin delivered through a pellet (SHAMM) for 4 weeks, BDL for 4 weeks, and BDL plus 5 mg melatonin delivered through a pellet (BDLM) for 4 weeks. Their spatial memory was assessed using a Morris water-maze task. Plasma and brains were collected for biochemical and ADMA analyses. We found that the BDL group had significantly elevated levels of ADMA in the plasma, the prefrontal cortex, and the dorsal hippocampus, and worse spatial performance than that of the control groups. Melatonin administration prevented an increase in the ADMA levels in the plasma, prefrontal cortex, and dorsal hippocampus, and prevented spatial deficits in BDL rats. In addition, melatonin maintained brain-derived neurotrophic factor in the dorsal hippocampus at a level comparable with controls. We concluded that melatonin is effective in preventing spatial deficits and decreasing ADMA levels in the plasma, prefrontal cortex, and dorsal hippocampus in young BDL rats. Brain ADMA levels might play a role in BDL-induced spatial deficits.

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Section: Discussionmentioning

confidence: 75%

Melatonin prevented spatial deficits and increases in brain asymmetric dimethylarginine in young bile duct ligation rats

et al. 2018

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“… Hydroxylated pregnenolone sulphate N -acetylglucosamine isomer 1* Pregnenolone sulphate N -acetylglucosamine Pregnanediol sulphate N -acetylglucosamine Tauro(cheno) deoxycholic acid N -acetylglucosaminide * 5 UGT3A1 Blood metabolite levels, Primary biliary cholangitis (PBC) Neither the gene UGT3A1 nor the PBC has a known relationship to AD, although we note that a progressive cognitive impairment different to delirium is a feature of PBC, independently of liver pathology 40 , 41 . In animal models of biliary cirrhosis that has led to memory impairment, hippocampal pregnenolone sulphate infusion resulted in a memory-enhancing effect 42 . CM, gut microbiota 3-Aminoisobutyrate 5 AGXT2 Metabolite levels, Asymmetrical dimethylarginine levels, Symmetrical dimethylarginine levels Gut microbiota N,N,N -Trimethyl- l -alanyl- l -proline betaine 11 AND 21 Regulatory feature: ENSR00000961656 AND intergenic variant Butyryl or isobutyryl carnitine * 15 intergenic variant Trimethylamine 10 PYROXD2 General cognitive ability, Obesity-related traits, Metabolite levels l -Lysine 19 SLC7A9 Estimated glomerular filtration rate, Creatinine levels DNA methylation 5-Methylcytidine 4 …”

Section: Resultsmentioning

confidence: 99%

Urinary metabolic phenotyping for Alzheimer’s disease

Kurbatova

Garg

Whiley

et al. 2020

Sci Rep

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Finding early disease markers using non-invasive and widely available methods is essential to develop a successful therapy for Alzheimer’s Disease. Few studies to date have examined urine, the most readily available biofluid. Here we report the largest study to date using comprehensive metabolic phenotyping platforms (NMR spectroscopy and UHPLC-MS) to probe the urinary metabolome in-depth in people with Alzheimer’s Disease and Mild Cognitive Impairment. Feature reduction was performed using metabolomic Quantitative Trait Loci, resulting in the list of metabolites associated with the genetic variants. This approach helps accuracy in identification of disease states and provides a route to a plausible mechanistic link to pathological processes. Using these mQTLs we built a Random Forests model, which not only correctly discriminates between people with Alzheimer’s Disease and age-matched controls, but also between individuals with Mild Cognitive Impairment who were later diagnosed with Alzheimer’s Disease and those who were not. Further annotation of top-ranking metabolic features nominated by the trained model revealed the involvement of cholesterol-derived metabolites and small-molecules that were linked to Alzheimer’s pathology in previous studies.

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“…Serial dilutions of cDNAs were used for calculation of the efficiencies of the primer sets on real‐time PCR. In this regard, it was found that the efficiencies of the various primer sets were similar …”

Section: Methodsmentioning

confidence: 99%

Neuroprotective effects of various doses of topiramate against methylphenidate induced oxidative stress and inflammation in rat isolated hippocampus

Motaghinejad

Motevalian

Shabab

2016

Clin Exp Pharma Physio

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Methylphenidate (MPH) abuse causes neurodegeneration. The neuroprotective effects of topiramate (TPM) have been reported but its putative mechanism remains unclear. The current study evaluates the role of various doses of TPM on protection of rat hippocampal cells from MPH-induced oxidative stress and inflammation in vivo. Seventy adult male rats were divided into six groups. Group 1 received normal saline (0.7 mL/rat) and group 2 was injected with MPH (10 mg/kg) for 21 days. Groups 3, 4, 5, 6 and 7 concurrently were treated by MPH (10 mg/kg) and TPM (10, 30, 50, 70 and 100 mg/kg, intraperitoneally (i.p.)), respectively for 21 days. After drug administration, the open field test (OFT) was used to investigate motor activity. Oxidative, antioxidant and inflammatory factors were measured in isolated hippocampus. Also, the brain-derived neurotrophic factor (BDNF) level was measured by reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blotting. Cresyl violet staining of Dentate Gyrus (DG) and CA1 cell layers of the hippocampus were also performed. MPH significantly disturbs motor activity in OFT and TPM (70 and 100 mg/kg) decreased this disturbance. Also MPH significantly increased lipid peroxidation, mitochondrial reduced state of glutathione (GSH) level, interleukin (IL)-1β and tumour necrosis factor (TNF)-α and BDNF level in isolated hippocampal cells. Also superoxide dismutase, glutathione peroxidase and glutathione reductase activity significantly decreased. Various doses of TPM attenuated these effects and significantly decreased MPH-induced oxidative damage, inflammation and hippocampal cell loss and increased BDNF level. This study suggests that TPM has the potential to be used as a neuroprotective agent against oxidative stress and neuroinflammation induced by frequent use of MPH.

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The effects of intra-dorsal hippocampus infusion of pregnenolone sulfate on memory function and hippocampal BDNF mRNA expression of biliary cirrhosis-induced memory impairment in rats

Cited by 18 publications

References 62 publications

Melatonin prevented spatial deficits and increases in brain asymmetric dimethylarginine in young bile duct ligation rats

Melatonin prevented spatial deficits and increases in brain asymmetric dimethylarginine in young bile duct ligation rats

Urinary metabolic phenotyping for Alzheimer’s disease

Neuroprotective effects of various doses of topiramate against methylphenidate induced oxidative stress and inflammation in rat isolated hippocampus

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