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Alzheimer’s disease may be triggered by stress hormone

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Alzheimer’s disease may be triggered by stress hormone

According to researchers at Temple’s School of Medicine, Alzheimer’s disease may be triggered by steroids, which are hormones released by the adrenal glands in situations of stress. This could be a key trigger that underlies the mechanism of Alzheimer’s disease ( AD) with late onset.

The link between stress hormones and Alzheimer’s disease has been emphasized by previous studies that have shown that the level of corticosteroids is two to three times higher in AD patients compared to patients without AD. Domenico Pratico, professor of pharmacology and microbiology and immunology in Temple’s School of Medicine, who led the study, said that stress is an environmental factor that seem to have a role in causing Alzheimer’s disease. The explanation is that when you have elevated stress hormones for long time, they can cause neuronal cell death, which harms memory and learning. To investigate this hypothesis, Temple’s School of Medicine researchers have conducted several experiments to elucidate the mechanisms by which stress causes Alzheimer’s disease.

Alzheimer's

Alzheimer’s Disease

To perform these experiments, the researchers used triple transgenic mice that have developed the two hallmarks of Alzheimer’s disease, that is beta amyloid protein and the tau protein. One group of mice received injections with high levels of corticosteroid daily for a week to mimic stress. Researchers found no significant differences in terms of memory, but what they noticed was that tau protein was significantly increased in rats that received injections of corticosteroids. In addition, what is interesting is that the synapses, the connections between neurons, have been damaged or destroyed.

Pratico pointed out that this was surprising because they have not found memory or learning impairment although the pathology was visibly affected. The researchers also pointed out that another surprising result was that a third group of mice that were genetically engineered to lack the enzyme 5-lipoxygenase in the brain appeared to be immune and had no neurological damage from corticosteroid. Previous studies conducted by Pratico have shown that high levels of 5-lipoxygenase resulted in increasing levels of amyloid and tau protein in the brain regions responsible for memory and learning (that contribute to Alzheimer’s disease).

The conclusion was that corticosteroids use 5-lipoxygenase as a mechanism to injure synapses leading to learning and memory impairment, which are the main symptoms in AD. “So that is strong support for the hypothesis that if you block 5-lipoxygenase, you can probably block the negative effects of corticosteroid in the brain” added Pratico.