The suprachiasmatic nucleus is the part of the brain responsible for regulating the wake-sleep cycle, a cycle that is often disturbed in patients with dementia due to damage to this area of the brain. Bright light therapy is used as a treatment for a number of mental health conditions, including seasonal affective disorder, bipolar depression, chronic depressive disorder and insomnia. A brand new research at MIT suggests it may be useful for dementia, too. Bright light therapy has been seen to improve disturbances in the wake-sleep cycle of patients with dementia. Additionally, light therapy has been shown to reduce aggressive behavior in patients with Alzheimer’s disease or related dementia (ADRD). The study, which was published in the prestigious journal Neuronfound that bright light therapy (called GENUS) helped neurons and microglia (the brain immune cells) to remove amyloid plaques and inflammation. Preemptively, neurodegeneration was largely prevented with this method of treatment.
The light therapy reduced inflammation, enhanced synaptic function, and protected against cell death in mice models that were genetically programmed to develop Alzheimer’s. Previous study from the same team investigated the effects of LED lights flickering at specific frequencies and found that it significantly reduced beta-amyloid plaques found in the brain in mice models. The treatment was shown to induce brain waves called gamma oscillations that inhibited the generation of beta-amyloid plaques and increased the activity of cells that help to destroy these plaques. For the new study, the team used two different types of mice that had been genetically programmed to develop Alzheimer’s. One type of mouse had a mutated version of the Tau protein and was named Tau P301S, and the other was programmed to produce a protein called p25 and was named CK-p25. Mutations in tau are known to cause neurofibrillary tangles. Similarly, the p25 protein causes severe neurodegeneration.
The mice were given visual stimulation for one hour every day for three to six weeks. After three weeks of treatment, neurodegeneration was not seen in Tau P301S mice. In comparison, tau P301S mice that had not been given light treatment had lost 15-20% of their neurons. CK-p25 mice were treated for six weeks and also showed no neurodegeneration.Further investigation revealed that in the neurons of mice not treated with light therapy, the expression of genes linked to DNA repair, synaptic function and vesicle trafficking (a process key to proper synaptic function) was lower. Treated mice showed significantly higher expression in these genes, as well as higher numbers of synapses and greater brain wave synchrony between the different areas of the brain. After studying microglia, it was found that the gene expression of inflammatory proteins was increased in untreated mice, while decreasing in treated ones. The team confirmed this result by molecular biology techniques called transcriptomics and phospho-proteomics.
While this suggests that the microglia are key elements in combatting inflammation and reducing the number of molecules capable of forming both amyloid plaques and neurofibrillary tangles, the exact mechanism causing these beneficial changes is still unknown. Further studies into whether bright light therapy is effective in late-stage Alzheimer’s will now be carried out. Phase one clinical trials in humans have also started. Such studies will test the efficacy of light and sound stimulation in patients with Alzheimer’s. Li-Huei Tsai, senior author explained the amazing results of his research: ”I have been working with p25 protein for over 20 years and I know this is a very neurotoxic protein. We found that the p25 transgene expression levels are exactly the same in treated and untreated mice, but there is no neurodegeneration in the treated mice. I haven’t seen anything like that; it’s very shocking. A lot of scientists have been asking me whether the microglia are the most important cell type in this beneficial effect, but to be honest, we really don’t know. Yet.”
- Edited by Dr. Gianfrancesco Cormaci, PhD, specialist in Clinical Biochemistry.
Adaikkan C et al., Tsai LH. Neuron; 2019 May 2
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Dott. Gianfrancesco Cormaci
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