Neuroscience highlights in 2022: cytoskeletal transport

Sleigh, James N.; Schiavo, Giampietro

doi:10.1016/s1474-4422(22)00482-3

Cited by 1 publication

(3 citation statements)

References 11 publications

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“…Fahmy et al [28] report that the excess of inorganic forms of copper is toxic for cells on the account of stimulating excessive production of ROS. Moreover, the overabundance of copper can inactivate certain cellular enzymes, destroy mitochondrial protein complexes, modify low-density lipoproteins, and damage the DNA [10,29,30]. The results of our research showed that administering a diet enriched with CuNPs in a proportion of 6.5 mg/kg decreased the levels of GAChE and βAP and increased the level of AChE both in the brain and jejunum of rats.…”

Section: Discussionmentioning

confidence: 56%

“…The same authors demonstrated that copper has a strong affinity to tyrosine residues located at the N-terminus of βAP. The oxidative modification of N-terminus tyrosine residues caused by copper induces further oligomerization of βAP [30,32,[44][45][46]. This promotes the production of amyloid plaques and Tau protein tangles.…”

Section: Discussionmentioning

confidence: 99%

“…The low efficiency of oxidative phosphorylation decreases the production of ATP. As a result, it impairs neurometabolism and induces slow nerve cell death [30]. What is more, the complex of calmodulin and calcium synthesized in compliance with CAMK2a during protein kinase activation stimulates pathological protein phosphorylation on the mitochondrial membrane, including Tau protein [42][43][44].…”

Section: Discussionmentioning

confidence: 99%

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The Influence of Copper Nanoparticles on Neurometabolism Marker Levels in the Brain and Intestine in a Rat Model

Cendrowska-Pinkosz

Krauze

Juśkiewicz

et al. 2023

IJMS

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The aim of this study is to assess the effect of different forms and dosages of copper on the levels of markers depicting the neurodegenerative changes in the brain and the jejunum. The experiment was performed using 40 male Wistar rats fed a typical rat diet with two dosages of Cu used as CuCO3 (6.5 and 13 mg/kg diet) and dietary addition of two CuNP dosages (standard 6.5 and enhanced 13 mg/kg diet), randomly divided into four groups. The levels of neurodegenerative markers were evaluated. Nanoparticles caused a reduction in the level of glycosylated acetylcholinesterase (GAChE), an increase the level of acetylcholinesterase (AChE) and lipoprotein receptor-related protein 1 (LRP1), a reduction in β-amyloid (βAP) in the brain and in the intestine of rats and a reduction in Tau protein in the brain of rats. The highest levels of AChE, the ATP-binding cassette transporters (ABC) and LRP1 and lower levels of toxic GAChE, β-amyloid, Tau, hyper-phosphorylated Tau protein (p-Tau) and the complex of calmodulin and Ca2+ (CAMK2a) were recorded in the tissues of rats receiving a standard dose of Cu. The neuroprotective effect of Cu can be increased by replacing the carbonate form with nanoparticles and there is no need to increase the dose of copper.

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