Alzheimer’s disease is a neurodegenerative disorder that causes deterioration in communication, motor skills, intellectual deficiencies and severe memory loss. One of the main causes of the disease is the accumulation of a protein called amyloid β (Aβ) that clusters around neurons in the brain. it triggers their degeneration and hampers their activity.
Studies in animals have shown an increase in aggregation of β (Aβ) in the brain’s learning and memory centre – the hippocampus a decline in the transmission of signals of neurons. The degeneration affects the ‘synaptic plasticity’ of neurons. This is the ability of synapses to adapt to an increase or decrease in signalling activity. Synaptic plasticity is important for the development of cognitive functions and learning in the hippocampus. Therefore, β (Aβ) and its role in cognitive memory and deficits has been the main focus for most Alzheimer’s research, to find a treatment for the disease.
A team of scientists from Japan continued research based on this hypothesis. The study was led by Professor Akiyoshi Saitoh from Tokyo University of Science.
This particular study looked at Oxytocin, “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,” Prof Saitoh says.
Prof Saitoh’s group set out to connect the dots, realising this. The team of scientists used Aβ to perfuse slices of mouse hippocampus, to confirm that Aβ causes the neurons signalling ability to decline or impairs their synaptic plasticity. However, it was seen that additional perfusion of oxytocin helped increase the signalling abilities. This suggested that oxytocin can reverse the impairment of synaptic plasticity caused by Aβ.
Oxytocin facilitates certain cellular chemical activities
Oxytocin is known for facilitating certain cellular chemical activities important for strengthening formation of memories and neuronal signalling potential. Previous studies have shown that Aβ suppresses some of the chemical activities. When the scientists blocked these chemical activities, it was found that the addition of oxytocin to the hippocampal did not reverse the damage caused by Aβ to the synaptic plasticity. It was further found that oxytocin does not have a significant impact on synaptic plasticity in the hippocampus, however, it was somehow able to reverse the ill-effects of Aβ.
Prof Saitoh remarks,
“This is the first study in the world that has shown that oxytocin can reverse Aβ-induced impairments in the mouse hippocampus.”
He further concluded,
“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.”
