A naturally occurring brain protein appears able to slow or stop Alzheimer’s disease in recent studies done on animal models.The brain’s entorhinal cortex, which supports memory, normally produces brain-derived neurotrophic factor (BDNF); however, its production appears to decrease when Alzheimer’s is present. When researchers injected BDNF in lab animals that either were aged, had entorhinal cortex damage or were genetically altered to have Alzheimer’s-like symptoms, they found that the animals had improved memory and cognitive skills and that cell degeneration and death was prevented or reversed.

“The effects of BDNF were potent,” researcher Dr. Mark Tuszynski, professor of neurosciences at the University of California, San Diego, School of Medicine, said in a news release issued by the school. “When we administered BDNF to memory circuits in the brain, we directly stimulated their activity and prevented cell death from the underlying disease.”

The animals receiving the treatment — transgenic mouse models of Alzheimer’s disease, aged rats, rats with induced damage to the entorhinal cortex, aged rhesus monkeys and monkeys with entorhinal cortex damage — also showed long-term benefits. They began producing more BDNF on their own and exhibited better brain cell signaling and neuronal function, whereas the untreated animals degenerated further. The hippocampus, the brain’s short-term memory processing center, which Alzheimer’s disease can quickly damage, also appeared to show improvement.

The team, whose findings were published in the Feb. 8 issue of Nature Medicine, concluded that, since BDNF appeared both safe and effective on animal models, it could hold hope for treating Alzheimer’s disease in humans.

“In this series of studies, we have shown that BDNF targets the cortical cells themselves, preventing their death, stimulating their function and improving learning and memory,” Tuszynski said. “Thus, BDNF treatment can potentially provide long-lasting protection by slowing, or even stopping, disease progression in the cortical regions that receive treatment.”

(Source: University of California, San Diego, news release, Feb. 8, 2009)