Sci. Aging Knowl. Environ., 8 September 2004
Will a Filet a Day Keep the Neurologist Away?
Fish oil molecule forestalls neuron damage in Alzheimer's mice
People who eat lots of fish might protect their brain from Alzheimer's disease (AD), and new work helps explain why. Depriving mice of a fatty acid in fish stresses cells and sunders the neural links that transmit information through the brain.
The brains of AD patients teem with tangles of the protein tau and goopy plaques of amyloid (see "Detangling Alzheimer's Disease"), but how the disease steals memory remains elusive. Forgetfulness might creep in because AD destroys synapses, the connections that allow brain cells to communicate. A fatty acid called docosahexaenoic acid (DHA) appears to be crucial for keeping synapses healthy. The membranes of brain cells--especially those portions at the synapse--bristle with DHA. The compound protects memory in rats engineered to develop AD, and one of its derivatives nurtures cells. What's more, several studies have found relatively low rates of AD among people who eat large amounts of DHA, which is found in oily fish such as tuna and mackerel. Neuroscientist Gregory Cole of the University of California, Los Angeles, and colleagues wanted to determine how DHA in the diet affects synapses in old mice engineered to amass amyloid.
The rodents nibbled either DHA-rich chow or food lacking the fatty acid. The researchers determined the effects on dendrites, the cell protrusions that receive neural impulses in synapses. After 5 months on the low-DHA diet, the amounts of two key dendrite proteins had plummeted; quantities of the same two proteins decline in AD brains. However, quantities of two proteins found on synapses' transmitting side remained constant. The imbalance suggests that without DHA, dendrites are breaking the synaptic connection, Cole says. The team also detected more proteins corroded by reactive oxygen species in the low-DHA animals, and these rodents produced less of a molecule that helps activate a neuron-protecting biochemical pathway. Learning difficulties accompanied these molecular woes: DHA-deprived mice exhibited poorer memory in a maze. Together, the results suggest that depleting DHA provokes cell damage, severs synapses, and hinders memory. So hiking the amount of DHA we eat might help fend off AD, Cole says. Not many brain cells died in the experiment, Cole notes, indicating that some of the mice's memory problems--and maybe those of AD patients--might be fixable if dendrites could be refurbished.
"This study is important because it adds to the evidence that cold-water ocean fish, a good source of DHA, are indeed good brain food, just as grandmother said," says neurochemist Lloyd Horrocks of Ohio State University in Columbus. The work "provides a very strong demonstration of the protective properties of DHA," adds neuroscientist Nicolas Bazan of the Louisiana State University Health Sciences Center in New Orleans. Before people rush to the fish market, though, he cautions that "the brain regulates DHA uptake in a way we don't understand," so gorging on tuna and mackerel might not jack up quantities of brain DHA. Fish can also contain toxic substances such as mercury. Safely boosting the amount of DHA might net fewer cases of AD.
September 8, 2004
Science of Aging Knowledge Environment. ISSN 1539-6150