In laboratory brain tissue studies, oxytocin appeared to reverse the effect of a toxic protein associated with Alzheimer’s disease on brain cells. In addition, the hormone can restore the plasticity of cells, which is crucial for memory and learning. Researchers at Tokyo University recently investigated whether the chemical could help protect nerve cells in the early stages of Alzheimer’s disease.
Oxytocin effect in cognitive decline
The hormone oxytocin comes from part of the brain, the hypothalamus. It plays an important role in childbirth, breastfeeding and social bonding. Oxytocin can also facilitate romantic bonding. The body releases the hormone during sexual activity and earns the chemical its popular reputation as a “love hormone”. However, Oxytocin’s related role in social attachment also suggests that it could also help treat social anxiety and autism. Its effect on memory is less well known, but a study in mice found that it can improve long-term spatial learning and memory. Alzheimer’s disease is the most common form of dementia and affects millions of people worldwide. Those suffer from progressive memory loss and cognitive decline. A leading theory suggests that the accumulation of lumps of a toxic protein called beta-amyloid in the brain causes Alzheimer’s. But recent research has questioned this view.
An older study found that injecting synthetic beta-amyloid into the brain of rats caused learning and memory problems. Other research has shown that scientists inhibit long-term potentiation (LTP), in which nerve cells can code memories. This occurs when different nerves simultaneously strengthen the electrical connections (synapses) that transmit signals between them. So beta-amyloid appears to affect the ability of nerve cells to strengthen their synapses in this way. Neuroscientists refer to this as nerve plastic. The hippocampus is involved in the formation of new memories and may be particularly susceptible to this damage. In the most recent study, researchers in Japan confirmed for the first time that perfusion of brain cells from the hippocampi of mice with beta-amyloid inhibits LTP, thereby reducing the plasticity of the cells. However, they then discovered that the oxytocin effect appears to reverse this impairment.
New research experiment
In order to investigate whether oxytocin was directly involved in restoring the plasticity of the nerve cells, the researchers carried out another experiment. Before perfusing the mouse brain tissue with beta-amyloid, they pre-treated it with a chemical. This blocks the receptors for oxytocin on nerve cells. As predicted, the oxytocin effect could no longer restore the lost nerve plastic after this pretreatment. For this reason, the scientists suspect that oxytocin could have a potential to treat the memory loss associated with Alzheimer’s disease.
There are currently no sufficiently satisfactory drugs to treat dementia, and new therapies with novel mechanisms of action are desired. Alzheimer’s is a complex, poorly understood disease that gradually develops over the course of several years. Much more work will be required to test the restorative effects of oxytocin on nerve plastic surgery in live animals. If successful, efforts would likely move to human clinical research. The researchers found in their work that a major obstacle to the development of viable treatment is the fact that the blood-brain barrier interferes with the passage of oxytocin into the brain.