Effect of memantine on expression of Bace1-as and Bace1 genes in STZ-induced Alzheimeric rats
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ORIGINAL ARTICLE
Effect of memantine on expression of Bace1‑as and Bace1 genes in STZ‑induced Alzheimeric rats Parisa Azadfar1 · Zahra Noormohammadi1 · Maryam Noroozian2,3 · Akram Eidi1 · Pejman Mortazavi4 Received: 4 April 2020 / Accepted: 26 June 2020 © Springer Nature B.V. 2020
Abstract Recent studies have showed that the long non-coding RNAs (lncRNAs) expression is dysregulated in different neurodegenerative disorders like Alzheimer’s disease (AD). In the present study, the effects of memantine on the level of Bace1-as and Bace1 genes’ expression in streptozotocin (STZ)-induced Alzheimer’s and memantine treated rats were investigated. The male Wistar rats were randomly divided into four groups: 1-Normal control, 2-Sham-operated control, 3- Alzheimer’scontrol rats (ICV-STZ), 4-Experimental group rats treated by memantine in a dose of 30 mg/kg/day for 28 days in ICV-STZ rats. The expression of Bace1-as and Bace1 genes was measured by quantitative-PCR in the brain and blood tissues. ELISA was used to analyze Bace1 and Aβ proteins. Expression of Bace1-as was significantly increased in the brain and blood tissues of the experimental group (p = 0.032 and p = 0.034, respectively). The expression of Bace1 gene showed no significant changes in the brain. Furthermore, the ELISA analysis revealed that Bace1 protein was significantly increased in the plasma of the Alzheimer’s control group (p = 0.000) and in the brain tissue of the experimental group (p = 0.000). Additionally, Aβ levels had no significant changes between all groups studied. The Bace1 protein may be used as a prognostic biomarker in plasma, or before using memantine as a treatment. Furthermore, Bace1-as gene expression may play a role in monitoring the progression of AD. Keywords Alzheimer’s disease · Bace1 gene · Bace1-as lncRNA · Rat · STZ · Memantine · Plasma biomarker
Introduction Alzheimer’s disease (AD) is characterized by extracellular amyloid plaques, intracellular-neurofibrillary tangles (NFTs) and neuropathological loss. The amyloid plaques and NFTs modify synaptic plasticity, leading to synapse loss [1, 2]. The important component of amyloid plaques is an amyloid beta peptide (Aβ), 36–42 amino acids, which is prone to accumulation, and NFTs are aggregation of hyperphosphorylated tau protein [3, 4].The Aβ is a small fragment of * Zahra Noormohammadi z‑[email protected]; [email protected] 1
Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran
2
Memory and Behavioral Neurology Department (MBND), Roozbeh Hospital, Tehran, Iran
3
Department of Neuroscience, School of Advanced Technologies in Medicine, Tehran, Iran
4
Department of Pathobiology, Science and Research Branch, Islamic Azad University, Tehran, Iran
amyloid precursor protein (APP) cleaved by the two proteases β and γ-secretase in the amyloidogenic pathway, and both are membrane proteins. APP in the non-amyloidogenic pathway cleaved by α—and γ –secretase [5]. Therefore, β –secretase is essential for Aβ formation [6] and is encoded
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