Alzheimer’s disease is a neurodegenerative disease that is the most common form of senile dementia. It is characterised by cognitive and particularly mnesic disorders that seriously affect the quality of life of the patient and those around him and often lead to the patient being placed in a specialised institution. The disease is estimated to affect around 35 million people worldwide, including 10 million in Europe due to the ageing population and the risk factor for age. The global cost of the medical and societal care of Alzheimer’s disease was estimated in 2010 at $604 billion and could reach more than $1.1 trillion in 2030. Four drugs are now marketed in the therapeutic management of Alzheimer’s disease: three inhibitors of acetylcholinesterase (galantamine REMINYL®, rivastigmine EXELON® and donepezil ARICEPT®), as well as an NMDA receptor antagonist (EBIXA® memantin). They essentially produce only a symptomatic effect without calling into question the evolution of the disease, which has led the High Authority of Health in France to judge their therapeutic interest in terms of benefit-risk and to question their reimbursement. However, their sales amounted to more than $2.7 billion worldwide in 2014. The relative ineffectiveness of current treatments and the fall in the public domain of patents has sparked intense global competition and hundreds of molecules have been the subject of clinical studies. These concern approaches targeting the main biological targets involved in the pathogenesis of Alzheimer’s disease (amyloid peptide, tau protein, inflammation, cholinergic system, neurotransmitters...). Unfortunately many of these studies have failed, although currently there are still more than 150 clinical trials involving mainly small molecules, but also immunotherapy approaches. As these abilities are impaired during the course of Alzheimer’s disease, we consider that donecoprid, or another agent reproducing its pleiotropic Swiss knife character, could be of symptomatic interest in the treatment of Alzheimer’s disease, restoring cholinergic neurotransmission in a sustainable way thanks to its neuroprotective effect. The neurotrophic effect, which is also manifested by the donecprid, could, on the other hand, be capable of halting the course of the disease by allowing even partial recovery of altered cognitive functions and perhaps avoiding the institutionalisation of patients, which is so cumbersome in terms of the cost to public health and suffering for companions.