3 MIN READ | Neuropsychology

‘Love Hormone’ Oxytocin Could Be Used to Treat Cognitive Disorders Like Alzheimer’s

Psychreg

Cite This
Psychreg, (2020, July 20). ‘Love Hormone’ Oxytocin Could Be Used to Treat Cognitive Disorders Like Alzheimer’s. Psychreg on Neuropsychology. https://www.psychreg.org/oxytocin-treat-alzheimers/
Reading Time: 3 minutes

 183 total views,  2 views today

Alzheimer’s disease is a progressive disorder in which the nerve cells (neurons) in a person’s brain and the connections among them degenerate slowly, causing severe memory loss, intellectual deficiencies, and deterioration in motor skills and communication. One of the main causes of Alzheimer’s is the accumulation of a protein called amyloid β (Aβ) in clusters around neurons in the brain, which hampers their activity and triggers their degeneration.

Studies in animal models have found that increasing the aggregation of Aβ in the hippocampus, the brain’s main learning and memory centre, causes a decline in the signal transmission potential of the neurons therein. This degeneration affects a specific trait of the neurons, called ‘synaptic plasticity‘, which is the ability of synapses (the site of signal exchange between neurons) to adapt to an increase or decrease in signalling activity over time. Synaptic plasticity is crucial to the development of learning and cognitive functions in the hippocampus. Thus, Aβ and its role in causing cognitive memory and deficits have been the focus of most research aimed at finding treatments for Alzheimer’s.

Now, advancing this research effort, a team of scientists from Japan, led by Professor Akiyoshi Saitoh from the Tokyo University of Science, has looked at oxytocin, a hormone conventionally known for its role in the female reproductive system and in inducing the feelings of love and well-being.

‘Oxytocin was recently found to be involved in regulating learning and memory performance, but so far, no previous study deals with the effect of oxytocin on Aβ-induced cognitive impairment,’ Professor Saitoh says. Realising this, Professor Saitoh’s group set out to connect the dots. Their findings are published in Biochemical and Biophysical Research Communication.

Professor Saitoh and team first perfused slices of the mouse hippocampus with Aβ to confirm that Aβ causes the signalling abilities of neurons in the slices to decline (or in other words) impairs their synaptic plasticity. Upon additional perfusion with oxytocin, however, the signalling abilities increased, suggesting that oxytocin can reverse the impairment of synaptic plasticity that Aβ causes.

To find out how oxytocin achieves this, they conducted a further series of experiments. In a normal brain, oxytocin acts by binding with special structures in the membranes of brain cells, 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. Expectedly, when the receptors were blocked, oxytocin could not reverse the effect of Aβ, which shows that these receptors are essential for oxytocin to act.

Oxytocin is known to facilitate certain cellular chemical activities that are important in strengthening neuronal signalling potential and formation of memories, such as influx of calcium ions. Previous studies have suspected that Aβ suppresses some of these chemical activities. When the scientists artificially blocked these chemical activities, they found that addition of oxytocin addition to the hippocampal slices did not 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 is somehow able to reverse the ill-effects of Aβ.

Professor Saitoh remarks: ‘This is the first study in the world that has shown that oxytocin can reverse Aβ-induced impairments in the mouse hippocampus.’

This is only a first step and further research remains to be conducted in vivo in animal models and then humans before sufficient knowledge can be gathered to reposition oxytocin into a drug for Alzheimer’s. But, Prof Saitoh remains hopeful. He concludes: ‘At present, there are no sufficiently satisfactory drugs to treat dementia, and new therapies with novel mechanisms of action are desired. Our study puts forth the interesting possibility that oxytocin could be a novel therapeutic modality for the treatment of memory loss associated with cognitive disorders such as Alzheimer’s disease. We expect that our findings will open up a new pathway to the creation of new drugs for the treatment of dementia caused by Alzheimer’s disease.’

***

Image credit: Freepik


Disclaimer

Psychreg is mainly for information purposes only. Materials on this website are not intended to be a substitute for professional advice, diagnosis, medical treatment, or therapy. Never disregard professional psychological or medical advice nor delay in seeking professional advice or treatment because of something you have read on this website.

We work with different advertisers and sponsors to bring you free and quality content. We cannot be held liable for the actions of any of these vendors. Any links provided on this website to other websites are not intended to provide an endorsement, approval, recommendation or preference by Psychreg. We have no liability or responsibility whatsoever for the privacy practices or the content of those linked websites whatsoever.

We publish differing views and we foster freedom of expression. Opinion pieces on this website do not reflect the views of the editor or any of our contributors.

We aim to create a platform where people can better understand each other.  If you have an alternative view on any of the articles that we published, please email: drelojo.howell@gmail.com

Read our full disclaimer here

Copy link