Oxytocin helps treat cognitive impairment

Alzheimer’s disease is a progressive disorder in which the nerve cells (neurons) in the human brain and the connections between them are slowly degenerated, causing severe memory loss, intellectual disability, and deterioration of motor ability and communication.

One of the main causes of Alzheimer’s disease is the accumulation of a protein called amyloid beta (Aβ) in clusters around neurons in the brain. This blocks neuronal activity and causes degeneration.

Studies in animal models have shown that increasing Aβ aggregation in the hippocampus, the main learning and memory center of the brain, reduces the neuronal signaling potential therein.

This degeneration affects a specific property of neurons called “synaptic plasticity.” This is the ability of the synapse, the place of signal exchange between neurons, to adapt to increasing or decreasing signaling activity over time. Synaptic plasticity is important for hippocampal learning and cognitive development.

Therefore, Aβ and its role in causing cognitive memory and impairment have been the focus of most research aimed at finding treatments for Alzheimer’s disease.

To advance the efforts of this research, a team of Japanese scientists, led by Professor Akiyoshi Saito of Tokyo University of Science, is currently working on a hormone known to induce the role of female reproductive system and emotion of love. I am paying attention to oxytocin which is and happiness.

Oxytocin has recently been shown to be involved in the regulation of learning and memory capacity, but so far no previous studies have addressed the effects of oxytocin on Aβ-induced cognitive impairment.

Akiyoshi Saitoh, Professor, Tokyo University of Science

To achieve this, Professor Saito’s group set out to connect the dots. Their findings are Biochemical and biophysical research communication..

Professor Saito and his team first perfused mouse hippocampal slices with Aβ and found that Aβ impairs the signaling capacity of neurons in the slices, impairing synaptic plasticity.

However, further perfusion with oxytocin increases its signaling capacity, suggesting that oxytocin can reverse the Aβ-induced impairment of synaptic plasticity.

To find out how oxytocin accomplishes this, they conducted a further series of experiments. In the normal brain, oxytocin acts by binding to a special structure of the brain cell membrane called the oxytocin receptor.

Scientists artificially “blocked” these receptors in mouse hippocampal slices to see if oxytocin could reverse the Aβ-induced impairment of synaptic plasticity without binding to these receptors. .. As expected, oxytocin was unable to reverse the effects of Aβ when the receptor was blocked. This indicates that these receptors are essential for the action of oxytocin.

Oxytocin is known to promote certain cytochemical activities that are important in enhancing neuronal signaling capacity and memory formation, such as calcium ion influx. Previous studies have suspected that Aβ suppresses some of these chemical activities.

When scientists artificially blocked these chemical activities, they found that the addition of oxytocin supplementation to hippocampal slices did not reverse the damage to synaptic plasticity caused by Aβ. Furthermore, they found that oxytocin itself does not affect hippocampal synaptic plasticity, which somehow can reverse the adverse effects of Aβ.

“This is the first study in the world to show that oxytocin can reverse Aβ-induced damage in the hippocampus of the mouse,” said Saito. This is only the first step, and further studies in vivo in animal models and humans are needed before collecting sufficient knowledge to relocate oxytocin to Alzheimer’s drug.

However, Professor Saito still hopes. “Currently, there are no satisfactory drugs to treat dementia, and new therapies with new mechanisms of action are desired. Our study shows that for the treatment of oxytocin-related amnesia. It has interesting potential that could be a new treatment with cognitive impairment such as Alzheimer’s disease.

“We expect our findings to open new avenues for the creation of new drugs for the treatment of dementia caused by Alzheimer’s disease.”