'Love hormone' oxytocin could be used to treat cognitive disorders like Alzheimer's

Date:
July 20, 2020
Source:
Tokyo University of Science
Summary:
Alzheimer's disease progressively degrades a person's memory and
cognitive abilities, often resulting in dementia. Amid efforts to
find novel treatments for this disease, a recent breakthrough study
shows that oxytocin -- the hormone that we commonly know to induce
feelings of love and well-being -- can also effectively reverse
some of the damage caused by amyloid plaques in the learning and
memory center of the brain in an animal model of Alzheimer's.



FULL STORY ========================================================================== Alzheimer's disease progressively degrades a person's memory and
cognitive abilities, often resulting in dementia. Amid efforts to
find novel treatments for this disease, a recent breakthrough study
by scientists from Japan shows that oxytocin―the hormone that we
commonly know to induce feelings of love and well-being―can also effectively reverse some of the damage caused by amyloid plaques in the learning and memory center of the brain in an animal model of Alzheimer's.


========================================================================== 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 b (Ab)
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 Ab in the hippocampus―the brain's main learning and memory center―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 signaling activity over time. Synaptic plasticity is
crucial to the development of learning and cognitive functions in
the hippocampus. Thus, Ab 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 Ab-induced cognitive impairment," Prof Saitoh
says. Realizing this, Prof Saitoh's group set out to connect the dots.

Prof Saitoh and team first perfused slices of the mouse hippocampus
with Ab to confirm that Ab causes the signaling abilities of neurons
in the slices to decline or―in other words―impairs their
synaptic plasticity. Upon additional perfusion with oxytocin, however,
the signaling abilities increased, suggesting that oxytocin can reverse
the impairment of synaptic plasticity that Ab 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 Ab―induced impairment of
synaptic plasticity without binding to these receptors. Expectedly, when
the receptors were blocked, oxytocin could not reverse the effect of Ab,
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 signaling potential and
formation of memories, such as influx of calcium ions. Previous studies
have suspected that Ab 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 Ab. 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 Ab.

Prof Saitoh remarks, "This is the first study in the world that
has shown that oxytocin can reverse Ab-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."

========================================================================== Story Source: Materials provided by Tokyo_University_of_Science. Note:
Content may be edited for style and length.


========================================================================== Journal Reference:
1. Junpei Takahashi, Daisuke Yamada, Yudai Ueta, Takashi Iwai,
Eri Koga,
Mitsuo Tanabe, Jun-Ichiro Oka, Akiyoshi Saitoh. Oxytocin reverses
Ab- induced impairment of hippocampal synaptic plasticity in mice.

Biochemical and Biophysical Research Communications, 2020; 528
(1): 174 DOI: 10.1016/j.bbrc.2020.04.046 ==========================================================================

Link to news story: https://www.sciencedaily.com/releases/2020/07/200720093308.htm

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