The principal focus of this project is to describe the molecular mechanisms that cells utilize for membrane assembly and disassembly. Previous reports have presented evidence showing that membrane lipid bilayer assembly is a critical phenomenon in which the growth temperature is a critical point. The critical temperature T has now been demonstrated for the total lipid extracts of B. stearothermophilus, E. coli human red blood cells, rat brain, and the optic nerve of squid (Loligo). These studies span cell temperatures ranging from 15-60 C. From the critical bilayer assembly theory two conditions are predicted to cause membrane bilayer structure degeneration: a) when cell temperature is raised with membrane lipid composition kept constant, and b) when membrane lipid composition is modified at constant cell temperature. The first condition of membrane degeneration has now been demonstrated with studies of red blood cells under conditions of pyrexia. Hemolysis has been observed even when temperatures are elevated only 1 degree above 37 C; no hemolysis is detected at 37 C. The measured activation energy for hemolysis is consistent with theoretical calculations for membrane bilayer degeneration based on critical state theory. For testing the second condition for membrane degeneration (modification of membrane lipids) a comparison has been made of critical bilayer assembly for lipid extracts of tissue from Alzheimer's disease brains. Extracted lipids obtained from tissues with lesions characteristic of the disease do not assemble membrane bilayers at body temperature, while the lipids from tissue free of lesions assemble membrane bilayers at body temperature. From the perspective of the critical bilayer assembly theory these experiments indicate that a defect in the lipids obtained from Alzheimer lesions will cause membrane bilayer breakdown. The chemical nature of the lipid defect is currently under examination.
