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Using Light To Retrieve Lost Memories For Alzheimer’s Patients

Lost memories might be brought back by light stimulation of brain cells. The paper is published in Nature.

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While Alzheimer’s disease is characterised by great memory deficits, it is unclear as to whether the memories in question are forever lost. Nor is the causal reason of the disease documented: is it the consequence of faulty memory formation and storage or does it entail a problem with memory retrieval? Elucidating this question is believed to be the key to treatment because memory retrieval might be restored.

A new research attempts to answer these perplexing questions. The findings show that memory retrieval might be the starting point of the disease.

Memory retrieval has been linked with a specific group of neurones called DG neurones located in the dentate gyrus of the hippocampus. This was found after conditioning mice to fear a certain experience. The activation of the DG neurones happens through an experience, and they are later used to remember the said experience.

Mice of two groups (normal ones, and those engineered to exhibit impaired long-term memory) were exposed to a traumatic experience (electric shock to the foot). When this happened, they would freeze. They were put in the same container the next day, and the normal mice would remember what had happened previously and freeze. However, those showing early symptoms of Alzheimer’s did not.

The ‘Alzheimer’s rats’ then had their DG neurones engineered to respond to blue light. They put in the box and shocked again. Then, following several instances of exposure to blue light, these mice had their memories back as was shown when they were put in the container the next day and they froze. On the other hand, when all other neurons in the same region as the DG cells were activated, the treatment did not yield the previous results.

These findings show that the activation of DG neurones would restore their ability to have the long-term memories back.

The researchers, however, add that humans might not generate the same effects as the mice have. Furthermore, their work is limited in the sense that it only concerns the beginning of the disease, and complications regarding the maintenance and storage of the memory might still happen in later phases of the disease.

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