Neurodegenerative disorders are complicated, fatal conditions that degrade over time. miRNAs have been related by many studies to the appearance and progression of neurodegenerative diseases, as well as the development and flexibility of the nervous system (Quinlan et al. 2017). One of the primary pathological marks of Alzheimer’s disease is Aβ deposition, which is formed by plaques and insoluble protein presences, including Aβ42 and Aβ40. As a possible and valuable biomarker for AD diagnosis, a number of study suggested that Aβ may be employed. In the the time being, the primary biological protein that retains microtubules in neuronal axons stable is tau protein. Tau protein may be loose from Alzheimer’s disease neurons more often as a result of neuroaxial degeneration. Dysfunctional tau protein then folds to form the proximal axoplasm’s neurofibrillary tangles. Accordingly, elevated levels of phosphorylated tau protein (p-tau181, p-tau217, and p-tau231) in the cerebrospinal fluid and axoplasm, such as P-Tau181, 217, and 231, possibly will help as biomarkers for AD (Quinlan et al. 2017). Microglia and additional forms of neuro-inflammation, such as chronic inflammation, are important biomarkers of AD disease. Sialic acid-binding Ig-like lectin 3 (CD33), ephrin type-A receptor 1 (EPHA1), membrane-spanning 4-domains (MS4), activating receptor are expressed on myeloid cells 2 (TREM2), and ATP-binding holder sub-family A member 7 (ABCA7) are just an insufficient of the abundant genes that have been highly found to be highly expressed in Alzheimer’s disease. It has been revealed that miRNAs mixed up in Alzheimer’s diseases have the capability to control gene expression through binding to mRNA and either hindering translation or affecting its degradation, or preventing the synthesis of proteins or triggering the breakdown of targeted mRNA in addition to the above-mentioned biomarkers. Also, because of miRNAs are persistent in body circulation, they are also constant when packed down. Many neurodegenerative disorders may ultimately result from dysregulated microRNAs transcripts with high expression and improper variation (Sonntag 2010).
Alzheimer’s disease is the one of the most fatal neurodegenerative disorder, digonosis by clinical symptoms inculuding cognitive decline, personality changes, and progressive memory loss (Alzheimer’s 2016). Medically, AD is noticeable by neuronal degeneration in the hippocampus and cortex area of the brain, the accumulation of neurofibrillary tangles, and “senile plaques” containing Aβ-amyloid (Lane et al. 2018). Investigation recommends that apoptosis may play a important role in the neuronal degeneration detected in AD, with a important number of neurons suffering programmed cell death in the brains of patients with this condition (Caccamo et al. 2017). Some microRNAs involved in apoptosis, including miR-16 and miR-15, are known to control the human anti-apoptotic BCL-2 gene (Cimmino et al. 2005). Also, it has been proposed that the levels of miR-9, miR-128, and miR-1256 are significantly higher in the brains of AD patients associated to those in the brains of healthy adults (Sethi and Lukiw 2009). According to Wang et al. (2008a, b), there is a solid relationship between the severity of AD and the level of miR-107 expression levels, which failures with the progression of the disease. The step at which Aβ-amyloid is considered is governed by the enzyme beta-secretase 1 (BACE1), and miRNAs alike miR-328 and miR-298 can control BACE1 levels to effect the amount of Aβ-amyloid that is formed. The miR-328 and miR-298, which regulator BACE1 levels, can identify specific sites on the enzyme (Boissonneault et al. 2009).