## 1 Introduction  
Alzheimer's disease (AD) is characterized by progressive cognitive and memory deficits, and is among the most common public health problems worldwide [1]. Abnormal accumulation of amyloid beta (\(\mathsf{A}\beta\)) is widely accepted as a key driving factor for the pathogenesis of AD in the brain [2]. In the amyloidogenic pathway, \(\mathsf{A}\beta\) is produced from the cleavage of the amyloid precursor protein (APP) via the activation of \(\beta\)- and \(\gamma\)-secretase in the brain [3]. \(\mathsf{A}\beta\) accumulates in the extracellular region and forms amyloid plaque, which leads to neurotoxicity in patients with AD [4]. In addition, \(\mathsf{A}\beta\) induces several negative effects, such as neuroinflammation/lamation, oxidative stress, and neuronal apoptosis [5]. Oxidative stress induced by the over-production of reactive oxygen species (ROS) stimulates neuroinflammation/lamation via releasing inflammatory mediators and cytokines [6]. Furthermore, oxidative stress and neuroinflammation lead to neuronal apoptosis via the upregulation of pro-apoptotic factors [5, 7]. Therefore, the regulation of oxidative stress and neuroinflammation is crucial in the inhibition of \(\mathsf{A}\beta\) progression.  
Stem cells are undifferentiated cells that maintain homeostasis through differentiation and regeneration of cells in the body [8]. Adult stem cells have the ability to differentiate into multiple cell types and possess anti-inflammatory activity; therefore, they are considered for the treatment of heart disease, diabetes mellitus, and others [9]. Recently,many studies have focused on the effects of stem cells for the treatment of AD. Adult stem cells improve cognitive impairment and memory deficits by reducing A\(\beta\) deposition and enhancing the rate of A\(\beta\) clearance in an AD mouse model [10,11]. However, adult stem cells used for the treatment for AD encounter high cellular immune rejection by the human immune system due to the presence of antigens on their membranes, resulting in an extremely high economic burden due to their usage [12,13].  
Membrane-free stem cell extract (MFSCE) is produced by the removal of membranes from adult stem cells using patented technology to overcome the disadvantage of cellular immune rejection [14]. MFSCE is composed of components of adult stem cells from human adipose tissue, so it is associated with several biological activities, such as metabolic processes and biological regulation [14]. In previous studies, we demonstrated several beneficial effects of MFSCE [14,15]. The MFSCE attenuated inflammatory reaction by decreasing nitric oxide (NO) production in lipopolysaccharideacharide (LPS)-induced RAW264.7 cells [14]. The MFSCE indicated antioxidant activity via the elevation of antioxidant proteins in LLC-PK\({}_{1}\) cells [15]. However, the neuroprotective effect of MFSCE against neurotoxicity has not yet been investigated. In the present study, the protective effect of MFSCE against neurotoxicity in neuronal cells induced by A\(\beta\) was investigated. To understand the mechanisms underlying the neuroprotective effect of MFSCE, factors related to oxidative stress, neuroinflammation, neuronal apoptosis, and amyloidogenic pathway were evaluated in neuronal cells.