Besides, pro-apoptotic function in AD pathogenesis, de novo over-expression of Snca in hippocampus neuron after treatment with LA have a number of its neuroprotective effects such as tau substitution act in cellular transport, cellular localization,vesicle trafficking, membrane stability, cooperation with clathrin and amphiphysin to increase endocytosis, regulation of neurotransmitter transport, membrane depolarization, positive regulation of transmission of nerve impulse, regulation of post synaptic membrane potential, and finally act as oxidoreductase and antioxidant enzyme. This evidence concerns the gene SNCA and Alzheimer disease.