Omega-3 supplements protect against Alzheimer's in mice

Studies in mice shed some light on how dietary supplements of
omega-3 fatty acids might protect against Alzheimer's disease.

Previous research has linked fish oil supplements, high in DHA, with a reduced risk of Alzheimer's disease in people and other studies have found a low concentration of DHA in the blood of Alzheimer's patients.

But little is known about how this protection might arise and whether such supplements might really help Alzheimer's patients or those at genetic risk for the disease.

Greg Cole and colleagues from the University of California, Los Angeles (UCLA) tested the effects of dietary depletion or enhancement of the essential fatty acid docosahexaenoic acid (DHA) on transgenic mice engineered to have the human version of a mutant amyloid precursor protein (APP)-the source of the brain-clogging protein in Alzheimer's disease.

When the researchers restricted dietary fatty acids in the transgenic mice, they detected a decreased level of DHA in the brains of the transgenic animals compared to normal mice.

They also detected a comparative increase in damage to the dendrites, structural proteins on neurons that take in chemical signals from neighbouring neurons to trigger nerve impulses.

And they saw evidence that reduced DHA caused increased oxidative stress in the transgenic animals, which could cause damage. When they supplemented the animals with DHA, however, they found a protection against such damage.

In behavioural studies, the researchers also found that the transgenic mice on low-DHA diets showed 'profound performance deficits' in learning and remembering the location of hidden, submerged platforms in a tank called the Morris water maze. Supplementing the mice with DHA, however, prevented this deficit.

"The present results provide, for the first time, evidence that the combination of genetic (mutant human APP) and environmental risk factors (dietary essential fatty acids) for Alzheimer's can act synergistically to quantitatively reduce synaptic proteins, specifically, dendritic scaffold proteins, that are critical for cognition as evidenced by memory deficits observed in the Morris water maze paradigm,"​ write the researchers in the 2 September issue of Neuron (volume 43, no 5, pp 633-645).

"The results show a dramatic impact of diet on the expression of the Alzheimer's disease-related postsynaptic marker phenotype and provide new insight into how essential fatty acid intake may modulate the expression of neurodegenerative diseases, including AD,"​ they wrote.

The researchers also wrote that their findings "suggest that patients bearing a genetic risk of AD may be more vulnerable to a lack of essential fatty acids,"​ which tend to be reduced in the brain both in normal againg and Alzheimer's disease.

They concluded that their findings "support the idea that increased DHA intake should be considered as a potential neuroprotective strategy for Alzheimer's disease".

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