{"id":3561,"date":"2020-07-20T09:24:20","date_gmt":"2020-07-20T09:24:20","guid":{"rendered":"https:\/\/www.editage.com\/insights\/love-hormone-oxytocin-could-be-used-to-treat-cognitive-disorders-like-alzheimers\/"},"modified":"2025-01-15T06:29:46","modified_gmt":"2025-01-15T06:29:46","slug":"love-hormone-oxytocin-could-be-used-to-treat-cognitive-disorders-like-alzheimers","status":"publish","type":"post","link":"https:\/\/www.editage.com\/insights\/love-hormone-oxytocin-could-be-used-to-treat-cognitive-disorders-like-alzheimers","title":{"rendered":"&#8220;Love hormone&#8221; oxytocin could be used to treat cognitive disorders like Alzheimer&#8217;s"},"content":{"rendered":"<p style=\"text-align:justify; margin:0in 0in 0.0001pt\"><span style=\"font-size:12pt\"><span style=\"text-justify:inter-ideograph\"><span style=\"font-family:&quot;Times New Roman&quot;,serif\"><span style=\"font-family:&quot;Calibri&quot;,sans-serif\">Alzheimer\u2019s disease is a progressive disorder in which the nerve cells (neurons) in a person\u2019s brain and the connections among them degenerate slowly, causing severe memory loss, intellectual deficiencies, and deterioration in motor skills and communication. <\/span><\/span><\/span><\/span><\/p>\n<p style=\"text-align:justify; margin:0in 0in 0.0001pt\">\u00a0<\/p>\n<p style=\"text-align:justify; margin:0in 0in 0.0001pt\"><span style=\"font-size:12pt\"><span style=\"text-justify:inter-ideograph\"><span style=\"font-family:&quot;Times New Roman&quot;,serif\"><span style=\"font-family:&quot;Calibri&quot;,sans-serif\">One of the main causes of Alzheimer\u2019s is the accumulation of a protein called amyloid \u03b2 (A\u03b2) 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 A\u03b2 in the hippocampus\u2014the brain\u2019s main learning and memory center\u2014causes a decline in the signal transmission potential of the neurons therein. This degeneration affects a specific trait of the neurons, called \u201csynaptic plasticity,\u201d 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, A\u03b2 and its role in causing cognitive memory and deficits have been the focus of most research aimed at finding treatments for Alzheimer\u2019s. <\/span><\/span><\/span><\/span><\/p>\n<p style=\"text-align:justify; margin:0in 0in 0.0001pt\">\u00a0<\/p>\n<p style=\"text-align:justify; margin:0in 0in 0.0001pt\"><span style=\"font-size:12pt\"><span style=\"text-justify:inter-ideograph\"><span style=\"font-family:&quot;Times New Roman&quot;,serif\"><span style=\"font-family:&quot;Calibri&quot;,sans-serif\">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. \u201c<i>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 A\u03b2-induced cognitive impairment<\/i>,\u201d Prof Saitoh says. Realizing this, Prof Saitoh\u2019s group set out to connect the dots.<\/span> <span style=\"font-family:&quot;Calibri&quot;,sans-serif\">Their findings are published in\u00a0<a href=\"https:\/\/doi.org\/10.1016\/j.bbrc.2020.04.046\" style=\"color:blue; text-decoration:underline\">Biochemical and Biophysical Research Communication<\/a><span class=\"MsoHyperlink\" style=\"color:blue\"><span style=\"text-decoration:underline\">.<\/span><\/span><\/span><\/span><\/span><\/span><\/p>\n<p style=\"text-align:justify; margin:0in 0in 0.0001pt\">\u00a0<\/p>\n<p style=\"text-align:justify; margin:0in 0in 0.0001pt\"><span style=\"font-size:12pt\"><span style=\"text-justify:inter-ideograph\"><span style=\"font-family:&quot;Times New Roman&quot;,serif\"><span style=\"font-family:&quot;Calibri&quot;,sans-serif\">Prof Saitoh and team first perfused slices of the mouse hippocampus with A\u03b2 to confirm that A\u03b2 causes the signaling abilities of neurons in the slices to decline or\u2014in other words\u2014impairs their synaptic plasticity. Upon additional perfusion with oxytocin, however, the signaling abilities increased, suggesting that oxytocin can reverse the impairment of synaptic plasticity that A\u03b2 causes. <\/span><\/span><\/span><\/span><\/p>\n<p style=\"text-align:justify; margin:0in 0in 0.0001pt\">\u00a0<\/p>\n<p style=\"text-align:justify; margin:0in 0in 0.0001pt\"><span style=\"font-size:12pt\"><span style=\"text-justify:inter-ideograph\"><span style=\"font-family:&quot;Times New Roman&quot;,serif\"><span style=\"font-family:&quot;Calibri&quot;,sans-serif\">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 \u201cblocked\u201d these receptors in the mouse hippocampus slices to see if oxytocin could reverse A\u03b2-induced impairment of synaptic plasticity without binding to these receptors. Expectedly, when the receptors were blocked, oxytocin could not reverse the effect of A\u03b2, which shows that these receptors are essential for oxytocin to act. <\/span><\/span><\/span><\/span><\/p>\n<p style=\"text-align:justify; margin:0in 0in 0.0001pt\">\u00a0<\/p>\n<p style=\"text-align:justify; margin:0in 0in 0.0001pt\"><span style=\"font-size:12pt\"><span style=\"text-justify:inter-ideograph\"><span style=\"font-family:&quot;Times New Roman&quot;,serif\"><span style=\"font-family:&quot;Calibri&quot;,sans-serif\">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 A\u03b2 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 A\u03b2. 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 A\u03b2. <\/span><\/span><\/span><\/span><\/p>\n<p style=\"text-align:justify; margin:0in 0in 0.0001pt\">\u00a0<\/p>\n<p style=\"text-align:justify; margin:0in 0in 0.0001pt\"><span style=\"font-size:12pt\"><span style=\"text-justify:inter-ideograph\"><span style=\"font-family:&quot;Times New Roman&quot;,serif\"><span style=\"font-family:&quot;Calibri&quot;,sans-serif\">Prof Saitoh remarks, <i>\u201cThis is the first study in the world that has shown that oxytocin can reverse A\u03b2-induced impairments in the mouse hippocampus.\u201d<\/i> This is only a first step and further research remains to be conducted <i>in vivo<\/i> in animal models and then humans before sufficient knowledge can be gathered to reposition oxytocin into a drug for Alzheimer\u2019s. But, Prof Saitoh remains hopeful. He concludes, <i>\u201cAt 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\u2019s 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\u2019s disease.\u201d <\/i><\/span><\/span><\/span><\/span><\/p>\n<p style=\"text-align:justify; margin:0in 0in 0.0001pt\">\u00a0<\/p>\n<p style=\"margin:0in 0in 0.0001pt\"><span style=\"font-size:12pt\"><span style=\"font-family:&quot;Times New Roman&quot;,serif\"><b><span style=\"font-family:&quot;Calibri&quot;,sans-serif\">Reference<\/span><\/b><\/span><\/span><\/p>\n<p style=\"margin:0in 0in 0.0001pt\"><span style=\"font-size:12pt\"><span style=\"font-family:&quot;Times New Roman&quot;,serif\"><span style=\"font-size:11.0pt\"><span style=\"font-family:&quot;Calibri&quot;,sans-serif\">Title of original paper: Oxytocin reverses <\/span><\/span><span style=\"font-size:11.0pt\"><span style=\"font-family:&quot;Calibri&quot;,sans-serif\">A\u03b2-induced impairment of hippocampal synaptic plasticity in mice<\/span><\/span><\/span><\/span><\/p>\n<p style=\"margin:0in 0in 0.0001pt\"><span style=\"font-size:12pt\"><span style=\"font-family:&quot;Times New Roman&quot;,serif\"><span style=\"font-size:11.0pt\"><span style=\"font-family:&quot;Calibri&quot;,sans-serif\">Journal: <i>Biochemical and Biophysical Research Communications<\/i><\/span><\/span><\/span><\/span><\/p>\n<p style=\"margin:0in 0in 0.0001pt\"><span style=\"font-size:12pt\"><span style=\"tab-stops:130.5pt\"><span style=\"font-family:&quot;Times New Roman&quot;,serif\"><span style=\"font-size:11.0pt\"><span style=\"font-family:&quot;Calibri&quot;,sans-serif\">DOI: <\/span><\/span><span class=\"MsoHyperlink\" style=\"color:blue\"><span style=\"text-decoration:underline\"><span style=\"font-size:11.0pt\"><span style=\"font-family:&quot;Calibri&quot;,sans-serif\"><a href=\"https:\/\/doi.org\/10.1016\/j.bbrc.2020.04.046\" style=\"color:blue; text-decoration:underline\">10.1016\/j.bbrc.2020.04.046<\/a><\/span><\/span><\/span><\/span><\/span><\/span><\/span><\/p>\n<p class=\"Default\" style=\"margin:0in 0in 0.0001pt\">\u00a0<\/p>\n<p class=\"Default\" style=\"margin:0in 0in 0.0001pt\"><span style=\"font-size:12pt\"><span style=\"font-family:Calibri,sans-serif\"><span style=\"color:black\"><b>About <\/b><b>the Tokyo University of Science<\/b><\/span><\/span><\/span><\/p>\n<p style=\"text-align:justify; margin:0in 0in 0.0001pt\"><span style=\"font-size:12pt\"><span style=\"text-justify:inter-ideograph\"><span style=\"font-family:&quot;Times New Roman&quot;,serif\"><span style=\"font-family:&quot;Calibri&quot;,sans-serif\"><a href=\"https:\/\/www.tus.ac.jp\/en\/mediarelations\/\">Tokyo University of Science<\/a> (TUS) is a well-known and respected university, and the largest science-specialized private research university in Japan, with four campuses in central Tokyo and its suburbs and in Hokkaido. Established in 1881, the university has continually contributed to Japan&#8217;s development in science through inculcating the love for science in researchers, technicians, and educators. <\/span><\/span><\/span><\/span><\/p>\n<p style=\"text-align:justify; margin:0in 0in 0.0001pt\"><span style=\"font-size:12pt\"><span style=\"text-justify:inter-ideograph\"><span style=\"font-family:&quot;Times New Roman&quot;,serif\">\u00a0<\/span><\/span><\/span><\/p>\n<p style=\"text-align:justify; margin:0in 0in 0.0001pt\"><span style=\"font-size:12pt\"><span style=\"text-justify:inter-ideograph\"><span style=\"font-family:&quot;Times New Roman&quot;,serif\"><span style=\"font-family:&quot;Calibri&quot;,sans-serif\">With a mission of \u201cCreating science and technology for the harmonious development of nature, human beings, and society&#8221;, TUS has undertaken a wide range of research from basic to applied science. TUS has embraced a multidisciplinary approach to research and undertaken intensive study in some of today&#8217;s most vital fields. TUS is a meritocracy where the best in science is recognized and nurtured. It is the only private university in Japan that has produced a Nobel Prize winner and the only private university in Asia to produce Nobel Prize winners within the natural sciences field. <\/span><\/span><\/span><\/span><\/p>\n<p style=\"text-align:justify; margin:0in 0in 0.0001pt\">\u00a0<\/p>\n<p style=\"text-align:justify; margin:0in 0in 0.0001pt\"><span style=\"font-size:12pt\"><span style=\"text-justify:inter-ideograph\"><span style=\"font-family:Calibri,sans-serif\"><span style=\"color:black\"><b>About Professor Akiyoshi Saitoh from the Tokyo University of Science<\/b><\/span><\/span><\/span><\/span><\/p>\n<p class=\"Default\" style=\"text-align:justify; margin:0in 0in 0.0001pt\"><span style=\"font-size:12pt\"><span style=\"text-justify:inter-ideograph\"><span style=\"font-family:Calibri,sans-serif\"><span style=\"color:black\">Dr Akiyoshi Saitoh is a Professor at the Faculty of Pharmaceutical Sciences, Tokyo University of Science. A respected and senior researcher with more than 25 years of experience, he has more than 100 research publications to his credit and is the lead author of this paper. His chief areas of interest include medicinal pharmacology, behavioral pharmacology, and neuroscience, including the role of the amygdala in the fear extinction memory in rodents and the development of a novel opioid delta receptor agonist for antidepressants\/anxiolytics. He also has patents for drugs in this area. <\/span><\/span><\/span><\/span><\/p>\n<p class=\"Default\" style=\"text-align:justify; margin:0in 0in 0.0001pt\">\u00a0<\/p>\n<p class=\"Default\" style=\"text-align:justify; margin:0in 0in 0.0001pt\"><span style=\"font-size:12pt\"><span style=\"text-justify:inter-ideograph\"><span style=\"font-family:Calibri,sans-serif\"><span style=\"color:black\"><b>Media contact <\/b><\/span><\/span><\/span><\/span><\/p>\n<p class=\"Default\" style=\"text-align:justify; margin:0in 0in 0.0001pt\"><span style=\"font-size:12pt\"><span style=\"text-justify:inter-ideograph\"><span style=\"font-family:Calibri,sans-serif\"><span style=\"color:black\"><span style=\"font-size:11.0pt\">Tsutomu Shimizu <\/span><\/span><\/span><\/span><\/span><\/p>\n<p class=\"Default\" style=\"text-align:justify; margin:0in 0in 0.0001pt\"><span style=\"font-size:12pt\"><span style=\"text-justify:inter-ideograph\"><span style=\"font-family:Calibri,sans-serif\"><span style=\"color:black\"><span style=\"font-size:11.0pt\">Email: <\/span><span class=\"MsoHyperlink\" style=\"color:blue\"><span style=\"text-decoration:underline\"><span style=\"font-size:11.0pt\"><a href=\"mailto:mediaoffice@admin.tus.ac.jp\" style=\"color:blue; text-decoration:underline\">mediaoffice@admin.tus.ac.jp<\/a><\/span><\/span><\/span><\/span><\/span><\/span><\/span><\/p>\n","protected":false},"excerpt":{"rendered":"<p>Alzheimer\u2019s disease is a progressive disorder in which the nerve cells (neurons) in a person\u2019s brain and the connections among them degenerate slowly, causing severe memory loss, intellectual deficiencies, and deterioration in motor skills and communication. \u00a0 One of the main causes of Alzheimer\u2019s is the accumulation of a protein called amyloid \u03b2 (A\u03b2) in [&hellip;]<\/p>\n","protected":false},"author":1152,"featured_media":33313,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"inline_featured_image":false,"footnotes":""},"categories":[2435],"tags":[2482],"new_categories":[],"new_tags":[],"series":[],"class_list":["post-3561","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-trending-research","tag-science-update"],"acf":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v25.0 - https:\/\/yoast.com\/wordpress\/plugins\/seo\/ -->\n<title>&quot;Love hormone&quot; 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