Investigation into the brains of aged rhesus monkeys show damage in the white matter (the myelin sheath covering the axons), while the gray matter (the cell nuclei and dendrites in areas such as the frontal cortex and hippocampus)saa remain intact, according to research presented by Douglas Rosene, associate professor in the anatomy and neurobiology at Boston University at the Successful Aging Conference on June 1-4 in Madison, Wis. The greater the degree of damage Rosene found, the poorer the animals' performance on memory tasks. The neurons in the aged monkeys also were far slower in carrying impulses than those in younger animals. The findings, which he describes as preliminary, are based on a total of 80 rhesus monkeys equally divided between males and females. Rhesus monkeys are good models to study "normal" aging of the human brain because they don't develop Alzheimer's disease. "If we could find out what's damaging the white matter, we might be able to treat it," says Rosene. The damage may be the result of inflammation, he says, because microglial cells, the macrophages of the brain, are active. Should that prove to be the case, anti-inflammatory drugs, such as aspirin may help repair this damage.
From Hair to Eternity--of Keratin, Apes, and Humans
The fact that the human genome is nearly identical to those of hairier cousins suggests that a few genes may account for the differences. One candidate is a keratin gene that is silenced in humans, yet expressed in chimps and gorillas (H. Winter et al. "Human type I hair keratin pseudogene hHaA has functional orthologs in the chimpanzee and gorilla: evidence for recent inactivation of the human gene after the Pan-Homo divergence." Human Genetics 108:37-42, January 2001.) But human nakedness is likely a genetic accident, not a survival strategy. "The silencing of the gene did not represent an evolutionary advantage. It was just a new acquisition in an arising population that most probably represented our direct ancestors," says Jürgen Schweizer of the German Cancer Research Center in Heidelberg. The researchers sequenced one of 15 keratin genes, called hHaA, in people from several ethnic groups, including eight in Sub-Saharan Africa. All were homozygous for the mutation that squelches gene activity. The pervasiveness of the mutation supports the out-of-Africa hypothesis of human origins. "The mutation occurs in homozygous form in some of the oldest modern human populations, whose origin dates to about 170,000 years ago," explains Schweizer. A plausible scenario is that a small population in which the mutation arose remained isolated over many generations, so that carriers could have children together and produce homozygous individuals. "We believe that the time lapse between 240,000 and 170,000 years ago would have allowed this to occur," Schweizer adds.
