By blocking the action of IGF-1, the appearance of amyloid plaques is delayed and cognitive abilities are preserved for a longer time.
Decreasing the sensitivity of the brain to growth hormones would prevent Alzheimer’s disease. This discovery by a French team from Inserm has just been published in the scientific journal Brain.
Led by Martin Holzenberger from the Saint-Antoine Research Center (Paris), this work follows on from a previous publication. In 2008, researchers realized that by removing growth hormone receptors located on neurons, mice lived longer. The molecule in question is called IGF-1 (Insulin-like growth factor). Secreted by the liver, it stimulates the maturation of bones and organs, and plays a role in aging.
Slowed neurodegeneration
During this recent work, the research team wanted to know more about its action in the body, and its presumed role in neurodegenerative diseases such as Alzheimer’s.
To do this, they first blocked IGF-1 receptors in mouse neurons. Comparing them to “normal” mice, they observed that the brains of guinea pigs later presented lesions typical of Alzheimer’s disease, such as amyloid plaques. Their brains were also less subject to inflammation. By continuing the tests, the researchers also found a reduction in cognitive deficits.
Therapeutic track
For the authors, these observations show that the suppression of IGF-1 receptors has a neuroprotective effect. They also suggest the existence of a process of self-defense of neurons. The researchers suppose, in fact, that in the early stages of the disease a neuron succeeds in fighting against neurodegeneration. But this response turns out to be insufficient in the long term since the pathology evolves. They now hope to find out when this mechanism ceases to be effective.
This work will also contribute to the development of new therapeutic and preventive avenues against Alzheimer’s disease. But the road promises to be long and complex. “We cannot inhibit the IGF-1 receptor in the whole body because this hormone is essential for other cells,” explains Martin Holzenberger. On the other hand, specifically targeting neurons is a possibility. In any case, we need to learn more about how to take advantage of the good effects of IGF while avoiding the less good effects ”.
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