scholarly journals The effect of miR-101 on the memory of rats with a model of Alzheimer’s disease

2020 ◽  
Vol 11 (3) ◽  
pp. 354-359
Author(s):  
O. G. Berchenko ◽  
N. O. Levicheva ◽  
D. O. Bevzyuk ◽  
V. V. Sokolik

Memory impairment is a hallmark of Alzheimer’s disease. The clinical diagnosis of the disease is made in the later stages of its development, when specific therapy of the disease is not always effective. Therefore, the detection of early behavioral manifestations of memory disorders in the development of the disease will allow the use of preventive therapy aimed at stopping the death of neurons in brain structures. A neuroethological study of working, spatial, and emotional memory was performed in rats 15–16 months of age with a model of early manifestations of Alzheimer’s disease induced by stereotactic administration of β-amyloid peptide 40 aggregates into the hippocampus. Changes in the neuroethological components of working and spatial memory have been identified. Testing of working memory showed a violation in rats of recognizing the shape of identical objects, reducing experimental activity to unfamiliar objects and their differentiation. Spatial orientation disorders have been identified in the Barnes labyrinth. Emotional memory research has shown the preservation of innate forms of protective adaptive behaviour. At the same time, vegetative indicators reflected an increase in emotional tension. Intranasal administration of liposomal miRNA miR-101 involved in liposomes to rats with a model of early manifestations of Alzheimer’s disease improved neuroethological parameters of working and spatial memory. Restoration of the level of research activity and differentiation of familiar and unfamiliar objects in the testing of working memory in rats has been established. Spatial memory in Barnes labyrinth testing was improved by reproducing spatial orientation skills and relieving emotional stress. Thus, the intranasal use of miR-101 in Alzheimer’s disease is a promising approach to prevent the development of amyloidosis and preserve memory in the early manifestations of Alz-heimer’s disease.

2021 ◽  
Vol 15 ◽  
Author(s):  
Paola C. Bello-Medina ◽  
Fernando Hernández-Quiroz ◽  
Marcel Pérez-Morales ◽  
Diego A. González-Franco ◽  
Guadalupe Cruz-Pauseno ◽  
...  

The irreversible and progressive neurodegenerative Alzheimer’s disease (AD) is characterized by cognitive decline, extracellular β-amyloid peptide accumulation, and tau neurofibrillary tangles in the cortex and hippocampus. The triple-transgenic (3xTg) mouse model of AD presents memory impairment in several behavioral paradigms and histopathological alterations from 6 to 16 months old. Additionally, it seems that dysbiotic gut microbiota is present in both mouse models and patients of AD at the cognitive symptomatic stage. The present study aimed to assess spatial learning, memory retention, and gut microbiota alterations in an early adult stage of the 3xTg-AD mice as well as to explore its sexual dimorphism. We evaluated motor activity, novel-object localization training, and retention test as well as collected fecal samples to characterize relative abundance, alpha- and beta-diversity, and linear discriminant analysis (LDA) effect size (LEfSe) analysis in gut microbiota in both female and male 3xTg-AD mice, and controls [non-transgenic mice (NoTg)], at 3 and 5 months old. We found spatial memory deficits in female and male 3xTg-AD but no alteration neither during training nor in motor activity. Importantly, already at 3 months old, we observed decreased relative abundances of Actinobacteria and TM7 in 3xTg-AD compared to NoTg mice, while the beta diversity of gut microbiota was different in female and male 3xTg-AD mice in comparison to NoTg. Our results suggest that gut microbiota modifications in 3xTg-AD mice anticipate and thus could be causally related to cognitive decline already at the early adult age of AD. We propose that microbiota alterations may be used as an early and non-invasive diagnostic biomarker of AD.


2011 ◽  
Vol 500 ◽  
pp. e44-e45
Author(s):  
Revital Shani-Hershkovitch ◽  
Amit Reches ◽  
Dani Kerem ◽  
Noga Pinchuk ◽  
Naama Levy-Cooperman ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-17 ◽  
Author(s):  
Alessandra Masci ◽  
Roberto Mattioli ◽  
Paolo Costantino ◽  
Simona Baima ◽  
Giorgio Morelli ◽  
...  

β-Amyloid peptide (Aβ) aberrant production and aggregation are major factors implicated in the pathogenesis of Alzheimer’s disease (AD), causing neuronal deathviaoxidative stress. Several studies have highlighted the importance of polyphenolic antioxidant compounds in the treatment of AD, but complex food matrices, characterized by a different relative content of these phytochemicals, have been neglected. In the present study, we analyzed the protective effect on SH-SY5Y cells treated with the fragment Aβ25–35by two crude juices of broccoli sprouts containing different amounts of phenolic compounds as a result of different growth conditions. Both juices protected against Aβ-induced cytotoxicity and apoptotic cell death as evidenced by cell viability, nuclear chromatin condensation, and apoptotic body formation measurements. These effects were mediated by the modulation of the mitochondrial function and of theHSP70gene transcription and expression. Furthermore, the juices upregulated the intracellular glutathione content and mRNA levels or activity of antioxidant enzymes such as heme oxygenase-1, thioredoxin, thioredoxin reductase, and NAD(P)H:quinone oxidoreductase 1viaactivation of NF-E2-related factor 2 (Nrf2). Although the effects of the two juices were similar, the juice enriched in phenolic compounds showed a greater efficacy in inducing the activation of the Nrf2 signalling pathway.


2016 ◽  
Vol 1 (1) ◽  
Author(s):  
Tahereh Mahmoodzadeh ◽  
Maryam Haji Khasem Kashani ◽  
Hassan Ramshini ◽  
Alireza Moslem ◽  
Mohammad Mohammad-Zadeh

2005 ◽  
Vol 156 (2) ◽  
pp. 225-232 ◽  
Author(s):  
Elisa Ognibene ◽  
Silvia Middei ◽  
Stefania Daniele ◽  
Walter Adriani ◽  
Orlando Ghirardi ◽  
...  

2000 ◽  
Vol 48 (4) ◽  
pp. 567-579 ◽  
Author(s):  
Howard L. Weiner ◽  
Cynthia A. Lemere ◽  
Ruth Maron ◽  
Edward T. Spooner ◽  
Trelawney J. Grenfell ◽  
...  

2020 ◽  
Vol 9 (1) ◽  
pp. 17
Author(s):  
Ebrahim Esfandiari ◽  
Zeinab Shakerin ◽  
Shahnaz Razavi ◽  
Hojjatallah Alaei ◽  
Mustafa Ghanadian ◽  
...  

2021 ◽  
Vol 11 (10) ◽  
pp. 1300
Author(s):  
Stephanie L. Proskauer Proskauer Pena ◽  
Konstantinos Mallouppas ◽  
Andre M. G. Oliveira ◽  
Frantisek Zitricky ◽  
Athira Nataraj ◽  
...  

Before the course of Alzheimer’s disease fully manifests itself and largely impairs a patient’s cognitive abilities, its progression has already lasted for a considerable time without being noticed. In this project, we mapped the development of spatial orientation impairment in an active place avoidance task—a highly sensitive test for mild hippocampal damage. We tested vision, anxiety and spatial orientation performance at four age levels of 4, 6, 9, and 12 months across male and female TgF-344 AD rats carrying human genes for presenilin-1 and amyloid precursor protein. We found a progressive deterioration of spatial navigation in transgenic animals, beginning already at the age of 4 months, that fully developed at 6 months of age across both male and female groups, compared to their age-matched controls. In addition, we described the gradual vision impairment that was accentuated in females at the age of 12 months. These results indicate a rather early onset of cognitive impairment in the TgF-344 AD Alzheimer’s disease model, starting earlier than shown to date, and preceding the reported development of amyloid plaques.


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