Abstract
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.
Highlights
One of the first symptoms of Alzheimer’s disease is the irreversible deterioration of memory up to dementia
It has been shown that the neocortex and hippocampus (Insel & TakeharaNishiuchi, 2013; Huijgen & Samson, 2015) are structures that provide mechanisms for the formation of different types of memory: emotional, working, spatial (Silаchjov et al, 2008; Antunes & Biala, 2012; Grigоrchuk, 2013)
Administration to rats of aggregated β-amyloid peptide 40 in the hippocampus led to a gradual violation of the mechanisms of working memory
Summary
One of the first symptoms of Alzheimer’s disease is the irreversible deterioration of memory up to dementia. Alzheimer’s dementia is distinguished, which is due to the occurrence and course of cerebral amyloidosis (formation of a local excess of β-amyloid peptide (Aβ) aggregates in the foci of cholinergic neurons of the neocortex and hippocampus). The presence of a long asymptomatic period is a feature of neurodegenerative pathology of Alzheimer’s disease. During this period, the manifestations of specific disorders of memory and cognitive functions are compensated by the mechanisms of the brain (Purdenko, 2014). In patients with Alzheimer’s disease, it is the neurons of the neocortex and hippocampus that suffer the most from the toxicity of Aβ oligomers, which subsequently form senile plaques characteristic of amyloidogenic pathology (Mukhin, 2013). Violation of the mechanisms of consolidation of memory traces is observed already in the clinical stage of Alzheimer’s disease
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
