هورمون عشق می تواند به درمان آلزایمر کمک کند
بیماری آلزایمر به طور پیشرونده موجب زوال حافظه انسان و توانایی شناختی انسان شده و غالبا منجر به زوال عقل می‌شود.
نتیجه مطالعه اخیر نشان می‌دهد هورمون اُکسی‌توسین که معمولاً به هورمون عشق معروف است، می‌تواند برخی از آسیب‌های ناشی از پلاک‌‌های آمیلوئید را در مرکز یادگیری و حافظه مغز در مدل‌های حیوانی مبتلا به آلزایمر بازگرداند.
یکی از علل اصلی بیماری آلزایمر، انباشت پروتئینی موسوم به آمیلوئید بتا در دسته‌های در اطراف نورون‌های مغز است که فعالیت آن را مختل کرده و موجب نابودی آن‌ها می‌شود.
از این‌رو آمیلوئید بتا و نقش آن در بروز زوال شناختی و آلزایمر به اثبات رسیده است.
آکی‌یوشی سایتو سرپرست تیم تحقیق از دانشگاه توکیو، در این باره می‌گوید: ما دریافتیم که هورمون اُکسی‌توسین در تنظیم عملکرد یادگیری و حافظه دخیل است.
نتایج مطالعات نشان داد با تزریق اُکسی‌توسین بیشتر، توانایی‌های سیگنال دهی افزایش یافت که بیانگر آن است که این هورمون می‌تواند اختلال سیناپسی ناشی از آمیلوئید بتا را برگرداند.
TOKYO – Although scientists know many of the underlying symptoms which trigger Alzheimer’s disease, a cure remains elusive. Now, a new study suggests that oxytocin, a hormone best known for promoting feelings of love and wellbeing, may reverse some of the damage the degenerative illness causes.
Alzheimer’s disease is a progressive brain disease causing the continuous deterioration of mental functions. Its primary symptoms include severely impaired thinking, memory loss, and confusion.
One of the primary culprits in Alzheimer’s is a protein known as amyloid β (Aβ). Researchers say Aβ clumps together to form plaques around neurons in the brain. These plaque build-ups disrupt normal neuron function and triggers the degeneration.
A great deal of research focuses on the accumulation of Aβ plaques in the brain’s hippocampus. This region is believed to be the brain’s primary learning and memory center.
Studies find plaque clumps in the hippocampus disrupt a characteristic of neurons called synaptic plasticity, or the ability of brain synapses to adapt to different levels of neural activity over time. Synaptic plasticity is thought to play a crucial role in both learning and retaining memory.
Researchers at the Tokyo University of Science confirm Aβ impairs synaptic plasticity after examining plaque build-ups in mouse hippocampal slices. Their study then adds oxytocin to the animal’s brains, which reveals the hormone can reverse impairments to those synapses. When researchers block oxytocin receptors, they find oxytocin can’t reverse the damage of Aβ proteins, confirming the love hormone’s benefits.
The team believes oxytocin might also reverse this damage by impacting calcium activity. Oxytocin is known to facilitate calcium influx in cells, which is thought to play a key role in neural signaling and memory formation. Moreover, previous studies also suggest that Aβ might suppress calcium activity.
Based on these findings, researchers blocked the receptors responsible for calcium transport across cell membranes. When they did so, oxytocin was again unable to reverse the negative effects of Aβ on synaptic plasticity.
The study authors suggest that oxytocin can benefit the brain through both of these channels, reversing Aβ protein damage.
“This is the first study in the world that has shown that oxytocin can reverse Aβ-induced impairments in the mouse hippocampus,” says lead author Akiyoshi Saitoh in a media release. “At present, there are no sufficiently satisfactory drugs to treat dementia, and new therapies with novel mechanisms of action are desired.”
Saitoh adds oxytocin may give doctors hope of creating a drug which focuses on the memory disrupting effects of Alzheimer’s. The World Health Organization says there around 50 million people suffering with the disease across the globe.
“We expect that our findings will open up a new pathway to the creation of new drugs for the treatment of dementiacaused by Alzheimer’s disease.”
The study is published in the journalBiochemical and Biophysical Research Communication.
