Studies on membrane receptors and transmitter turnover have significantly advanced understanding of neuronal reactions. Structural and metabolic changes in nerve cells influence aging by altering neuronal and nervous system functions. Future research on molecular mechanisms of neuronal dysfunction in aging should focus on these changes. Questions remain about energy pathway redistribution in aging neurons and the relationship between membrane receptor and enzyme changes and phospholipid composition shifts during peroxide oxidation. Can changes in neuronal membrane protein synthesis and its relation to electric properties be a fundamental aging mechanism? Longevity is a genetically controlled trait. Gerontologists believe that differences in lifespan among species are genetically determined. However, this does not necessarily mean that lifespan differences within a species are genetically controlled. Genetic variations may affect lifespan, but accidental deaths due to genetic causes do not reflect normal lifespan. Sacher and Hart proposed two approaches to aging research: ontogenetic (molecular and cellular level) and phylogenetic (species differences). These approaches are attractive but not fully developed. The question of whether lifespan variations within a population are genetically controlled remains unanswered. A genetically controlled trait is an advanced stage of development controlled by genes. Longevity may be a complex trait influenced by many genes. Studies in Drosophila and humans show that major genes can affect lifespan, but no mutations have been found that prolong lifespan. These mutations are likely nonspecific and not related to lifespan control. Minor genes with additive effects may also influence lifespan. Studies on parent-offspring lifespan correlations suggest a small genetic influence. However, the exact role of minor genes in lifespan control is not yet clear. Research on these genes may provide insights into aging mechanisms.Studies on membrane receptors and transmitter turnover have significantly advanced understanding of neuronal reactions. Structural and metabolic changes in nerve cells influence aging by altering neuronal and nervous system functions. Future research on molecular mechanisms of neuronal dysfunction in aging should focus on these changes. Questions remain about energy pathway redistribution in aging neurons and the relationship between membrane receptor and enzyme changes and phospholipid composition shifts during peroxide oxidation. Can changes in neuronal membrane protein synthesis and its relation to electric properties be a fundamental aging mechanism? Longevity is a genetically controlled trait. Gerontologists believe that differences in lifespan among species are genetically determined. However, this does not necessarily mean that lifespan differences within a species are genetically controlled. Genetic variations may affect lifespan, but accidental deaths due to genetic causes do not reflect normal lifespan. Sacher and Hart proposed two approaches to aging research: ontogenetic (molecular and cellular level) and phylogenetic (species differences). These approaches are attractive but not fully developed. The question of whether lifespan variations within a population are genetically controlled remains unanswered. A genetically controlled trait is an advanced stage of development controlled by genes. Longevity may be a complex trait influenced by many genes. Studies in Drosophila and humans show that major genes can affect lifespan, but no mutations have been found that prolong lifespan. These mutations are likely nonspecific and not related to lifespan control. Minor genes with additive effects may also influence lifespan. Studies on parent-offspring lifespan correlations suggest a small genetic influence. However, the exact role of minor genes in lifespan control is not yet clear. Research on these genes may provide insights into aging mechanisms.