Alzheimer’s disease has long been associated with an unhealthy lifestyle based on a wrong diet, too much drinking and smoking. Now a new study confirms the idea, suggesting that eating the wrong diet could increase risk of developing Alzheimer’s. The study was conducted on mice and found a link between raised levels of the omega-6 fatty acid arachidonic acid and memory loss and behavioral changes, pointing to new strategies for tacking Alzheimer’s. Sources of omega-6 fatty acids include poultry, cereals, eggs, nuts, most vegetable oils and evening primrose oil. They are thought to be good for skin, hair, nails and hormonal balance.

Alzheimer’s is a degenerative disease for which there is no cure, as current drugs only ease its symptoms. The most common symptom is memory loss, as well as difficulty to remember recently learned facts. Sometimes, it can go undiagnosed for years. According to the estimates of the U.S. National Institutes of Health, there are currently about 5.2 million Americans with Alzheimer's disease. Globally, the disease affects more than 26 million people. One in 20 people with ages ranging from 65 to 74 and almost half of those with ages over 85 are affected by the terrible condition.

Arachidonic acid is released from phospholipids in the brain by an enzyme called group IVA phospholipase, or PLA2. By decreasing levels of PLA2 in Alzheimer’s mice using genetic engineering, the memory deficits and behavioral abnormalities associated with the disease were prevented, study leader Dr Rene Sanches-Mejia, from the Gladstone Institute of Neurological Diseases in San Francisco, California, US, (GIND) said.

“The most striking change we discovered in the Alzheimer mice was an increase in arachidonic acid and related metabolites in the hippocampus, a memory center that is affected early and severely by Alzheimer's disease. Arachidonic acid likely wreaks havoc in the Alzheimer mice by causing too much excitation, which makes neurons sick. By lowering arachidonic acid levels, we are allowing neurons to function normally,” he added.

The discovery has important therapeutic implications because it suggests that “inhibition of PLA2 activity might help prevent neurological impairments in Alzheimer's disease,” Co-author Dr Lennart Mucke, GIND director, said. However, more study needs to be done before testing this therapy on humans, he added.

The study was supported by the national Institutes of Health, the United States Department of Agriculture and the Gladstone Institutes. The findings were published in the Oct. 19 issue of the journal Nature Neuroscience.

Findings ways to cure Alzheimer’s is a top priority for researchers, as the number of patients with this condition is going to quadruple worldwide by 2050 reaching approximately 106 million cases. There are currently five drugs approved to treat Alzheimer’s, but they only mask symptoms for 6 to 12 months at most, according to the Alzheimer’s Association, an advocacy group based in Chicago.