Polyunsaturated fatty acids (PUFA), particularly arachidonic, eicosapentaenoic, dokosahexaenoic acids are the key structural elements of neuronal membranes. They constitute about 15-30% of the dry brain weight and that fact is largely responsible for the unique physical and chemical features of the neuronal phospholipid bilayers which cover many intracellular organelle and take part in information exchange processes. PUFA’s concentration changes in brain phospholipids infl uence many key cellular processes: membrane fl uidity, tertiary structure of receptor and transport proteins, receptor-ligand interacions and induce neurotransmission disturbances. Developing brain utilises vast quantities of PUFA’s, which are essential for neuronal development, migration, synaptogenesis, synaptic plasticity and neurogenesis. PUFA’s are also substrates for eicosanoids production, which are very short-living and extremely reactive substances playing many biological as well as signalling functions. Phospholipids processing by phospholipases is also connected with second messenger signalling activity and transduction of information received by many groups of metabotropic receptors. PUFAs concentration and metabolism disturbances have been observed repeatedly in schizophrenic patients. These changes were most frequent and intense on early stages of the disease. The above mentioned disturbances along with the key role of PUFAs in neurodevelopment and brain maturation contributed to the formulation of membrane phospholipids composition (MPC) hypothesis of schizophrenia, which may constitute a biochemical foundation for neuroimaging and neuronal cytoarchitecture disturbances observed in that chronic and devastating disease. The paper discusses the role of PUFA in brain, their metabolism and lipid abnormalities observed in schizophrenia. The main assumptions of David Horrobin’s MPC hypothesis of schizophrenia are also presented.