In laboratory studies using brain tissue, oxytocin appeared to reverse the effect of a toxic protein associated with Alzheimer’s disease on brain cells. The hormone may restore the cells’ “plasticity,” which is vital for memory and learning.
The hormone oxytocin originates in a part of the brain called the hypothalamus. Oxytocin plays important roles in childbirth, breastfeeding, and social bonding.
It may also
Its effect on memory is less well-established, but an older
Recently, researchers at Tokyo University of Science in Japan and Kitasato University, also in Tokyo, Japan, wondered whether or not the chemical could help protect nerve cells in the early stages of Alzheimer’s disease.
Alzheimer’s disease is the most common form of dementia, affecting more than
People with Alzheimer’s experience progressive memory loss and cognitive decline.
A leading theory proposes that the accumulation of clumps of a toxic protein called beta-amyloid in the brain causes Alzheimer’s. However, recent research has called this view into question.
One older study did find that injecting synthetic beta-amyloid into the brains of rats caused problems with learning and memory.
LTP occurs when different nerves fire simultaneously, strengthening the electrical connections, or “synapses,” that pass signals between them.
Beta-amyloid seems to impair nerve cells’ capacity to strengthen their synapses in this way, which neuroscientists refer to as their “plasticity.”
A part of the brain called the hippocampus, which is involved in the formation of new memories, may be particularly vulnerable to this damage.
In the latest study, the researchers in Japan first confirmed that perfusing brain cells from the hippocampi of mice with beta-amyloid inhibits LTP, thereby reducing the cells’ plasticity.
They then discovered that oxytocin appears to reverse this impairment.
To investigate whether or not oxytocin was directly involved in restoring the nerve cells’ plasticity, the researchers conducted a further experiment.
Before perfusing the mouse brain tissue with beta-amyloid, they pretreated it with a chemical that blocks oxytocin receptors on nerve cells.
As predicted, after this pretreatment, oxytocin was no longer able to restore the nerve cells’ lost plasticity.
“Oxytocin was recently found to be involved in regulating learning and memory performance, but so far, no previous study [has dealt] with the effect of oxytocin on [beta-amyloid-induced] cognitive impairment,” says study leader Prof. Akiyoshi Saitoh, from Tokyo University of Science.
“This is the first study in the world that has shown that oxytocin can reverse [beta-amyloid-induced] impairments in the mouse hippocampus.”
The findings appear in the journal Biochemical and Biophysical Research Communications.
The scientists propose that oxytocin could have potential as a treatment for the memory loss associated with Alzheimer’s disease.
“At present,” says Prof. Saitoh, “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,” he adds.
“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.”
– Prof. Akiyoshi Saitoh
So far, however, the research has only involved the acute effects of beta-amyloid and oxytocin on slices of brain tissue in the laboratory.
Alzheimer’s is a complex, poorly understood condition that develops gradually over the course of several years.
Much more work will be necessary to test the restorative effects of oxytocin on nerve plasticity in living animals. If successful, efforts would likely progress to clinical research in people.
The scientists note in their paper that a major stumbling block to the development of a viable treatment is the fact that the blood-brain barrier impairs the passage of oxytocin into the brain.