Alzheimer's disease (AD) is a neurodegenerative disease characterized by extracellular accumulation of amyloid plaques and intracellular accumulation of neurofibrillary tangles. Brain derived neurotrophic factor (BDNF) is the most abundant neurotrophic growth factor in the central nervous system. It is expressed in the hippocampus, cortex and basal forebrain, areas vital for learning, memory and executive function. The primary role of BDNF in the brain is to promote the survival of postmitotic neurons and the growth and differentiation of new neurons and synapses. Previous studies suggest the role of decreased BDNF levels in AD, where synapse and neuron loss and impaired memory are an essential part of the pathology. Amyloid beta (Aβ) affects BDNF levels directly, by inhibiting the proteolytic conversion of precursors to the final form, and indirectly by interfering with axonal transport. Given the protective effects of BDNF on neuronal toxicity induced by Aβ in vitro and in vivo, the use of BDNF represents a potential strategy for the treatment of AD. The aim of this study was to examine the potential effect of BDNF in the prevention of cell death, i.e. promoting the survival of neurons, using a primary culture of mouse cortical neurons treated with Aβ oligomers as an in vitro model of AD. The results of the study confirm the neuroprotective effect of BDNF and suggest that its use reduces apoptotic activity in an in vitro model of AD.