Oxytocin could be a potential new therapeutic option for cognitive disorders such as Alzheimer’s disease, suggests a team of scientists from the Tokyo University of Science. The team found that oxytocin could reverse the amyloid β (Aβ)-induced impairments in the mouse hippocampus which may help restore the cognitive function.
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. Accumulation of a protein called amyloid β (Aβ) in clusters around neurons in the brain, is one of the main causes of Alzheimer’s disease which in turn hampers their activity and triggers their degeneration.
The aggregation of Aβ in the hippocampus, affects the “synaptic plasticity,” of the neurons in the brain’s main learning and memory centre, causing a decline in the signal transmission potential of the neurons therein and thereby the cognitive functions.
Oxytocin is a peptide hormone and neuropeptide that is normally produced in the hypothalamus and released by the posterior pituitary. The peptide which is also known as ‘love hormone’ plays a role in social bonding, sexual reproduction, childbirth, and the period after childbirth. It is also known to facilitate certain cellular chemical activities that are important in strengthening neuronal signalling potential and formation of memories, such as the influx of calcium ions.
In a normal brain, oxytocin acts by binding with special structures in the membranes of brain cells, called oxytocin receptors.
During the study, Professor Akiyoshi Saitoh and team perfused slices of the mouse hippocampus with Aβ to confirm that Aβ aggregation affected the signalling abilities of neurons impairing the 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.
The scientists then artificially “blocked” the oxytocin receptors in the mouse hippocampus slices to see if oxytocin could still reverse Aβ-induced impairment of synaptic plasticity without binding to these receptors. However, as expected oxytocin could not reverse the effect of Aβ when the receptors were blocked, which shows that these receptors are essential for oxytocin to act.
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. “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,” said the researchers.
“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,” concluded Prof. Saitoh.