Scientists discover for the first time that oxytocin might be a possible new therapeutic option for cognitive disorders like Alzheimer’s disease.
Existing treatment regimens for Alzheimer’s are able to reduce the progression rate of memory degradation, but a recent breakthrough study from Japan has shown that Oxytocin- a hormone that’s commonly known for inducing feelings of love and well-being has an ability to reverse some of the damages made by amyloid plaques in the memory centre of the brain of animal models.
Alzheimer’s disease is a progressive disorder during which the nerve cells (neurons) in a person’s brain and therefore the connections among them degenerate slowly, causing severe dementia, intellectual deficiencies, and deterioration in motor skills and communication to the point where, in the long run, the person forgets how to walk, write and read. A major pathway that leads to this degeneration is the deposition of amyloid β (Aβ) protein in clusters around the neurons which affects their activity and triggers their degeneration. This deposition begins years before the actual onset of symptoms. Studies in animal models have shown that aggregation of Aβ in the hippocampus(part of the brain responsible for memory, emotions, and learning) affects the signal transmission potential of its neurons. This in turn affects the synaptic plasticity of neurons, which is the ability of synapses(exchanges signals between neurons) to adapt to an increase or decrease in signaling activity. Thus, Aβ has been the point for research when looking for a better treatment for Alzheimer’s.
A team of scientists from Japan, led by Professor Akiyoshi Saitoh from the Tokyo University of Science, has looked at oxytocin after a recent discovery showing that it was involved in regulating learning and memory performance. Then they set out to find if it has any effect on Aβ-induced cognitive impairment.
The experiment involved perfusing slices of mouse hippocampus with Aβ to confirm that Aβ causes the signaling abilities of neurons in the slices to decline or―in other words―impairs their synaptic plasticity. However, on additional perfusion with oxytocin, the signaling abilities improved, suggesting that oxytocin can reverse the impairment of synaptic plasticity that Aβ causes.
To find out how oxytocin causes this reversal, they conducted another series of experiments. Normally, oxytocin exerts its function by binding to receptors in the brain called oxytocin receptors. The scientists artificially “blocked” these receptors in the mouse hippocampus slices to see if oxytocin could reverse Aβ―induced impairment of synaptic plasticity without binding to these receptors. But when the receptors were blocked oxytocin was unable to reverse the damage showing that the receptors are required for oxytocin to perform its function. But they also found that the addition of oxytocin to the hippocampal slices did not necessarily reverse the damage to synaptic plasticity caused by Aβ. Additionally, they found that oxytocin itself does not have any effect on synaptic plasticity in the hippocampus, but it can somehow able to reverse the ill-effects of Aβ.
As it is one of the first studies on the effects of oxytocin in Aβ-induced cognitive impairment, it does not provide information on how it improves the quality of life or about the long-term benefits and risks of such a method in a patient. Nevertheless, it gives hope that with further research and studies of the same on in vivo animal models and then humans, it has the capacity to be developed as a novel strategy for the treatment of Alzheimer’s disease.
Reference : Tokyo University of Science
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