Alzheimer's diease (AD) is a senile dementia characterized by amyloid plaques, neurofibrillary tangles and synaptic and cell loss. In AD cognitive processes are perturbed. In the present study we investigated the early phase of AD when Ab is still the oligomeric soluble species. In particular, nanomolar concentration of the 42 aminoacid form of the oligomeric peptide (Ab_1-42) activates the phosphorilation of P38MAPK, a mitogen-activated protein kinase playing an essential role in regulating many cellular processes including inflammation, stress stimuli and death. We investigated whether BDNF (Brain-Derived Neurotrophic Factor) prevents from Ab neurotoxic effects. Decreasing BDNF levels during AD is well known. We examined primary neuronal cell culture by immunocytochemistry techniques. A nanomolar Ab treatment lead both to morphological sufference signals and to a P38MAPK activation increase. This two suffercence signals are more evident after a micromolar Ab treatment. When pretreated with BDNF before Ab_1-42 exposure the cells show a basal levels of phosphorilated P38MAPK. Our data, then, identifing BDNF as a possible neuroprotective agent in AD early phases.