Original article Mutations in the exon 7 of Trp53 gene and the level of p53 protein in double transgenic mouse model of Alzheimer’s disease

Dorszewska, Jolanta; Oczkowska, Anna; Suwalska, Monika; Różycka, Agata; Florczak-Wyspiańska, Jolanta; Dezor, Mateusz; Lianeri, Margarita; Jagodzińśki, Paweł P.; Kowalczyk, Michal J.; Prendecki, Michał; Kozubski, Wojciech

doi:10.5114/fn.2014.41742

Cited by 16 publications

(11 citation statements)

References 56 publications

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“…Thus, the levels of intracellular Ca 2+ concentration and calcium-regulated enzymes (e.g. calpains, proteases, phospholipases) were found to be elevated in animal models of AD [24] as well as the brains of AD patients [47,48]. The "calcium hypothesis" was further supported by demonstrations that, during brain aging, the molecular processes responsible for Ca 2+ regulation were impaired.…”

Section: Introductionsupporting

confidence: 49%

Alzheimer’s amyloid-β peptide disturbs P2X7 receptor-mediated circadian oscillations of intracellular calcium

Wilkaniec¹,

Schmitt²,

Grimm³

et al. 2016

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Section: Introductionsupporting

confidence: 49%

Alzheimer’s amyloid-β peptide disturbs P2X7 receptor-mediated circadian oscillations of intracellular calcium

Wilkaniec¹,

Schmitt²,

Grimm³

et al. 2016

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“…According to Chen et al [7], the level of miR-107 is reduced in p53 mutated cell lines. Moreover, muta- tions in TP53 gene which are common in cancer [45] have been previously reported in the AD animal model [13], and in AD patients may lead to accumulation of damaged DNA [15]. Furthermore, the homo-or heterozygous AD patients with APOE E4 allele and low apoE levels are most exposed to oxidative modifications and changes in the miR-107 level.…”

Section: Discussionmentioning

confidence: 95%

APOE genetic variants and apoE, miR-107 and miR-650 levels in Alzheimer’s disease

Prendecki¹,

Florczak-Wyspiańska²,

Kowalska³

et al. 2019

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Alzheimer's disease (AD) is a progressive neurodegenerative dementia in adults. Pathogenesis of AD depends on various factors, including APOE genetic variants, apolipoprotein E (apoE) phenotype and oxidative stress, which may promote both DNA and RNA damage, including non-coding RNA (ncRNA). Among ncRNAs, microRNA (miRNA) is known to contribute to pathologic processes in AD. The aim of the study was to analyse the plasma concentration of apoE by ELISA as well as the plasma levels of miR-107 and miR-650 by qPCR in relation to APOE genetic variants and clinical features including the age of onset and dementia severity in 64 AD patients and 132 controls. Our data showed that a low apoE plasma concentration was a risk factor for developing AD (OR = 5.18, p = 6.58E-06) and was particularly pronounced in severe dementia (p < 0.001) and correlated with cognitive functions (R = 0.295, p = 0.020), similarly as the level of miR-650 (R = 0.385, p = 0.033). The presence of APOE E4 allele in both AD patients and controls led to a reduction in apoE, while APOE E3/E3 genotype was associated with an increased apoE concentration and level of miR-107 in AD (p < 0.05) which was inversely correlated with the number of APOE E4 alleles (R =-0.448, p = 0.009). Additionally, patients with the onset at 60-69 years of age showed a reduced level of miR-107 (p < 0.05, as compared to AD above 80 years of age). Changed levels of plasma apoE, miR-107 and miR-650 may be a marker of the neurodegenerative process in the course of AD, associated with amyloid β metabolism and inordinate cell cycle.

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“…It was the cellular gatekeeper for growth and division, and controled the death of neurons in hippocampus [41]. p53 was deposited in the brain of AD mice and patients, resulting in the degeneration [42] and apoptosis of neurons [43]. The increased level of SIRT1 accompanied with decreased level of ac-p53 and p53 was consistent with the reduced apoptosis in the hippocampus.…”

Section: Discussionmentioning

confidence: 99%

Resveratrol promotes hUC-MSCs engraftment and neural repair in a mouse model of Alzheimer’s disease

Wang

Yang

et al. 2018

Behavioural Brain Research

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Mesenchymal stem cell transplantation is a promising therapeutic approach for Alzheimer’s disease (AD). However, poor engraftment and limited survival rates are major obstacles for its clinical application. Resveratrol, an activator of silent information regulator 2, homolog 1 (SIRT1), regulates cell destiny and is beneficial for neurodegenerative disorders. The present study is designed to explore whether resveratrol regulates the fate of human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) and whether hUC-MSCs combined with resveratrol would be efficacious in the treatment of neurodegeneration in a mouse model of AD through SIRT1 signaling. Herein, we report that resveratrol facilitates hUC-MSCs engraftment in the hippocampus of AD mice and resveratrol enhances the therapeutic effects of hUC-MSCs in this model as demonstrated by improved learning and memory in the Morris water maze, enhanced neurogenesis and alleviated neural apoptosis in the hippocampus of the AD mice. Moreover, hUC-MSCs and resveratrol jointly regulate expression of hippocampal SIRT1, PCNA, p53, ac-p53, p21, and p16. These data strongly suggests that hUC-MSCs transplantation combined with resveratrol may be an effective therapy for AD.

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Original article Mutations in the exon 7 of Trp53 gene and the level of p53 protein in double transgenic mouse model of Alzheimer’s disease

Abstract: A b s t r a c t Alzheimer's disease (AD) leads to generation of β-amyloid (Aβ) in the brain. Alzheimer's disease model PS/APP

Cited by 16 publications

References 56 publications

Alzheimer’s amyloid-β peptide disturbs P2X7 receptor-mediated circadian oscillations of intracellular calcium

Alzheimer’s amyloid-β peptide disturbs P2X7 receptor-mediated circadian oscillations of intracellular calcium

APOE genetic variants and apoE, miR-107 and miR-650 levels in Alzheimer’s disease

Resveratrol promotes hUC-MSCs engraftment and neural repair in a mouse model of Alzheimer’s disease

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