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MIT plan to restore Alzheimer’s patients’ lost memories with lasers

April 2, 2017

Loss of memory is the painful part of Alzheimer’s disease. However, new research is throwing promising hints of methods that can rekindle memories after a successful experiment on mice that was conducted by doctoral student Dheeraj Roy at Massachusetts Institute of Technology.

Deep-brain stimulation (DBS) has been used as a treatment method for Alzheimer’s to help patients recover cognitive functions albeit temporarily.

However, deep-brain stimulation mainly helps Parkinson’s patients and it has been showing limited benefits to Alzheimer’s affected.

The turning point in the efforts at retrieving memory in Alzheimer’s has been the success of scientists in activating the cells at the hippocampi of mice where memory is stored to fire neurons in the brain with lasers.

In Roy’s trials with the optogenetic laser method, the hippocampus of a seven-month-old mouse with early Alzheimer’s was targeted.

Successful Laser Experiment On Mice

Roy targeted memory cells of the brain called engram cells with a gene as part of optogenetics. It was Channelrhodopsin gene that created pores in the neuron membranes and filled the cells with positively charged ions to fire the neurons.

The circuitry, however, in the brains of older mice was different, as they are packed with the protein plaques and needed a new approach.

By drilling a hole in the seven-month-old mouse’s skull and inserting fibre-optic cable, Roy stimulated the engram cells with light pulses and bolstered the synaptic connections between neurons to reignite memories to re-form.

“I think what deep-brain is doing is broadly strengthening many inputs to the hippocampus,” Roy said.

Roy is now working to address the challenge of finding out memory neurons to target and fire without any invasive fibre-optic cable.

Mice in the early stages of Alzheimer’s proved that it can add new memories and retrieve “forgotten” memories with a little help.

This holds promise for millions of Alzheimer’s patients worldwide and is a reminder that improving memory is possible beyond the modest gains coming from existing drugs.

Roy’s mice trials have now been appreciated.

“I thought that the results were both remarkable and exciting,” said Raymond Kelleher, assistant professor of neurology at Massachusetts General Hospital.

Kelleher said it stimulated interest in the neglected area of memory retrieval or recall.

Alzheimer’s Patients Looking For A Bio Marker

Meanwhile, the problem of Alzheimer’s not showing any biological signal until it erupts fully is bothering neuroscientists.

“Neurology researchers throughout the world are therefore on the hunt for a specific biomarker signal for Alzheimer’s,” said Peter Dal-Bianco, Alzheimer’s expert from MedUni Vienna.

Dal-Bianco said lack of biological markers to alert the onset of Alzheimer’s treatment is affecting treatment and delays it until the disease manifests clinically. The disease lies suppressed in people who appear as healthy.

He also said that the preventive solution is to screen people in risk groups from the mid-30s to diagnose the disease with 100 percent certainty or tell them that they face no risk.

It has been found that Tau proteins play a crucial role in material transport within neurons. They are important reference points for assessing whether they are hyperphosphorylated, resulting in functional disturbances with cell death in tow.

An immunotherapy for reducing harmful Tau proteins was tested under the Neurology Department in Graz and MedUni Vienna. The results have been promising and could lead to a vaccination against this Tau issue of Alzheimer’s.

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