27Allium roseum is an important medicinal and aromatic plant, specific to the North African flora 28 and a rich source of important nutrients and bioactive molecules including flavonoids and 29 organosulfur compounds whose biological activities and pharmacological properties are well known. 30 In the present study, the inhibition of amyloid beta protein toxicity by the ethanolic extract of this 31 plant is investigated for the first time. Preliminary biochemical analyses identified kaempferol and 32 Luteolin-7-o-glucoside as the more abundant phenolic compounds. The effects of A. roseum extract 33 (ARE) on amyloid beta-42 (Aβ 42 ) aggregation and aggregate cytotoxicity, were investigated by 34 biophysical (ThT assay, Dynamic light scattering and transmission electron microscopy) and cellular 35 assays (cytotoxicity, aggregate immunolocalization, ROS measurement and intracellular 36Ca 2+ imaging). The biophysical data suggest that ARE affects the structure of Aβ 42 peptide, inhibits 37 its polymerization, and interferes with the path of fibrillogenesis. The data with cultured cells shows 38 that ARE reduces Aß 42 aggregate toxicity by inhibiting aggregate binding to the cell membrane and 39 by decreasing both oxidative stress and intracellular Ca 2+ . Accordingly, ARE could act as a 40 neuroprotective factor against Aβ aggregate toxicity in Alzheimer's disease. 41 42 Alzheimer's disease. 3 44 1. Introduction 45 Alzheimer's disease (AD), the main cause of senile dementia, is a progressive 46 neurodegenerative disorder associated with cognitive impairment and loss of neuronal cells affecting 47 over 25 million people worldwide [1], thus representing a heavy economic burden and a major health 48problem. The pathology is characterized by the accumulation in the brain of amyloid-β peptide (Aβ) 49 and hyperphosphorylated tau protein mainly found as extracellular senile plaques and intracellular 50 neurofibrillary tangles, respectively [2]. Aβ oligomers overproduction caused by mutations in APP 51 and presenilins [3, 4] appears to be directly associated to cognitive dysfunction and neurodegeneration 52 in AD [5]. Accordingly, toxic Aβ oligomers production and/or interaction with nerve cells appear 53 useful targets to reduce neuronal cell dysfunction. Feart, Samieri [6] suggest that in most cases AD is 54 affected by a combination of genetic and environmental risk factors, including physical activity and 55 nutrition; in particular, increasing evidence indicates that diet plays an important role in AD. Several 56 studies have associated plant food (i.e., vegetables, fruits, legumes, and cereals) consumption to 57 reduced risk of AD [7, 8]. Moreover, traditional medicine is increasingly appreciated as a useful 58 approach to treat many illnesses, and large funds are invested to explore the therapeutic potential of 59 medicinal plants. Fortunately, the search of active compounds from nature prospers and the results 60 increasingly obtained confirm the need to better known the therapeutic potential of these natur...