آلزایمربیماری‌های مغز و اعصابدمانس

نتایج یک پژوهش: آلزایمر منشاء مغزی ندارد؛ آلزایمر بیماری همهٔ بدن

دانشمندان مدتهاست که تصور می کنند آلزایمر ناشی از نوعی کاستی در مغز است اما حالا تحقیقات جدید نشان می دهد که یک پروتئین کلیدی عامل ایجاد کننده این بیماری است و آن را از دیگر نواحی بدن به مغز انتقال می دهد. انتظار می رود که نتایج این تحقیق به تولید داروهای تازه ای بیانجامد که در نهایت روند پیشرفت بیماری را کند یا متوقف نمایند.

یکی از علائم مهم بیماری آلزایمر تجمع پروتئین های آمیلوئید بتا در مغز است که به آنها پلاک های آمیلوئید گفته می شود و می توانند باعث مرگ سلول های مغزی شوند و در نهایت کارکرد سیستم عصبی و حافظه را تحت تاثیر قرار دهند.

البته باید اشاره کنیم اخیرا پژوهش های امیدوارکننده ای در این باره انجام گرفته  که نشان می دهند با یک آزمایش خون ساده می توان تجمع این پروتئین ها را در خون تشخیص داد با این حال طبق آن مطالعات پروتئین مذکور منشاء مغزی داشته.

حالا اما تحقیق تازه ای توسط دانشمندان چینی و کانادایی در این باره انجام شده که نشان می دهد پروتئین آمیلوئید بتای تولید شده در دیگر بخش های بدن می توانند به مغز سرایت نموده و در تشدید علائم مشابه به آلزایمر نقش ایفا کنند.

این فرایند با استفاده از تکنیکی به نام parabiosis انجام شد که در آن دو اورگانیزم مجزا از طریق جراحی به هم متصل می شوند تا جریان خون عبور یافته از آنها مشترک شود. محققان برای این منظور یک موش عادی را به جفت آن که به صورت ژنتیکی مقدار بیشتری از این پروتئین در بدنش تولید می شد متصل کردند.

بعد از ۱۲ ماه جریان یافتن خون مشترک در بدن این دو موش، علائم آلزایمر در بدن موش سالم هویدا شد و ظاهرا پروتئین های دخیل در این امر به مغز جانور منتقل شده و به پلاک هایی بدل شده بودند که طیف وسیعی از علائم مشابه به آلزایمر را در آن ایجاد کرده بود.

دانشمندان به دنبال تولید دارویی برای دفع این پروتئین از طریق کلیه ها و کبد هستند.

با در نظر داشتن همین مساله دانشمندان باور دارند که آمیلوئید بتا احتمالا در خارج از مغز تولید می شود و در بروز آلزایمر دخیل است. این پروتئین در خارج از بدن و درون ماهیچه ها و رگ های خونی تولید می گردد و طبق فرضیات هرچه انسان سالخورده تر می شود حجم بیشتری از آن به درون مغز راه می یابد و جوانب مخرب آلزایمر را در بدن تقویت می نماید.

به گفته Weihong Song از دانشگاه بریتیش کلمبیا هرچه انسان سالخورده تر می شود مانع خونی-مغزی در بدنش نیز ضعیف تر می گردد و به همین خاطر حجم بیشتری از پروتئین مذکور به داخل مغز نفوذ می یابد و نقش نوعی مکمل را برای پروتئینی ایفا می کند که در داخل خود مغز  تولید می شود و از این طریق روند بیماری را سرعت می دهد.

حالا دانشمندان تلاش دارند با تولید دارویی این پروتئین را به جای مغز به سمت کلیه ها یا کبد هدایت نمایند تا دیگر در مغز تجمع پیدا نکند و از بدن خارج شود.

Does Alzheimer’s originate outside the brain?

New research suggests Alzheimer's disease could originate in parts of a body other than the brain
New research suggests Alzheimer’s disease could originate in parts of a body other than the brain
Andreus/Depositphotos

 

Scientists have long thought that Alzheimer’s disease originates in the brain, but new research suggests that a key protein that triggers the disease could be carried to the brain from elsewhere in the body. The research offers pathways to new drug therapies that could potentially stop or slow the disease without working directly on the brain.

One of the fundamental symptomatic causes of Alzheimer’s disease is an accumulation, or “clumping”, of amyloid beta proteins in the brain. These accumulations are called amyloid plaques and they smother brain cells, resulting in inhibited nerve function and impaired memory.

Several promising recent studies have shown the potential for an early-warning diagnostic blood test to be developed that identifies the build-up of these amyloid beta proteins in the bloodstream. But until now it was generally considered that the plaque-generating proteins responsible for Alzheimer’s were produced inside the brain.

A new study from Chinese and Canadian scientists shows that amyloid beta proteins produced in other parts of the body can in fact cross into the brain and contribute to Alzheimer’s-like symptoms.

The process was identified using a technique called parabiosis, where two separate organisms are surgically attached to share the same bloodstream. The researchers joined a normal mouse with a partner that was genetically modified to produce high levels of the amyloid beta protein.

Two mice a surgically attached so they share a bloodstream allowing scientists to explore where blood-traveling proteins can infiltrate the brain
Two mice a surgically attached so they share a bloodstream allowing scientists to explore where blood-traveling proteins can infiltrate the brain
UBC

After 12 months of connected blood circulation the normal mice connected had effectively “contracted” Alzheimer’s disease from their genetically-modified partner. The proteins had traveled into the brains of the normal mice and developed into plaques causing a variety of Alzheimer’s-like symptoms. Effects were noticed in the healthy mice after as little as four months.

The researchers suggest that this is the first proof that amyloid beta produced outside of the brain can in fact contribute to the disease. Outside of the brain, amyloid beta is also produced in muscles, blood platelets and blood vessels. The hypothesis is that as we get older more amyloid beta crosses into the brain, amplifying the degenerative aspects of Alzheimer’s.

“The blood-brain barrier weakens as we age,” says Weihong Song from the University of British Columbia. “That might allow more amyloid beta to infiltrate the brain, supplementing what is produced by the brain itself and accelerating the deterioration.”

The study suggest that drug therapies could be developed to target amyloid beta in the body and push it towards the kidneys or liver to clear it from a system before it can accumulate in the brain, which is a difficult target for drug treatments.

The research was published in the journal Molecular Psychiatry.

Source: University of British Columbia

 Alzheimer’s disease might be a “whole body” problem

Alzheimer’s disease, the leading cause of dementia, has long been assumed to originate in the brain. But research from the University of British Columbia and Chinese scientists indicates that it could be triggered by breakdowns elsewhere in the body.

The findings, published today in Molecular Psychiatry, offer hope that future drug therapies might be able to stop or slow the disease without acting directly on the brain, which is a complex, sensitive and often hard-to-reach target. Instead, such drugs could target the kidney or liver, ridding the blood of a toxic protein before it ever reaches the brain.

The scientists demonstrated this cancer-like mobility through a technique called parabiosis: Surgically attaching two specimens together so they share the same blood supply for several months.

Two mice a surgically attached so they share a bloodstream allowing scientists to explore where blood-traveling proteins can infiltrate the brain

A pair of surgically-joined mice.

UBC Psychiatry Professor Weihong Song and Neurology Professor Yan-Jiang Wang at Third Military Medical University in Chongqing attached normal mice, which don’t naturally develop Alzheimer’s disease, to mice modified to carry a mutant human gene that produces high levels of a protein called amyloid-beta. In people with Alzheimer’s disease, that protein ultimately forms clumps, or “plaques,” that smother brain cells.

Normal mice that had been joined to genetically modified partners for a year “contracted” Alzheimer’s disease. Dr. Song says the amyloid-beta traveled from the genetically-modified mice to the brains of their normal partners, where it accumulated and began to inflict damage.

Not only did the normal mice develop plaques, but also a pathology similar to “tangles” – twisted protein strands that form inside brain cells, disrupting their function and eventually killing them from the inside-out. Other signs of Alzheimer’s-like damage included brain cell degeneration, inflammation and microbleeds. In addition, the ability to transmit electrical signals involved in learning and memory – a sign of a healthy brain – was impaired, even in mice that had been joined for just four months.

Besides the brain, amyloid-beta is produced in blood platelets, blood vessels and muscles, and its precursor protein is found in several other organs. But until these experiments, it was unclear if amyloid-beta from outside the brain could contribute to Alzheimer’s disease. This study, Dr. Song says, shows it can.

“The blood-brain barrier weakens as we age,” says Dr. Song, a Canada Research Chair in Alzheimer’s Disease and the Jack Brown and Family Professor. “That might allow more amyloid beta to infiltrate the brain, supplementing what is produced by the brain itself and accelerating the deterioration.”

Dr. Song, head of UBC’s Townsend Family Laboratories, envisions a drug that would bind to amyloid-beta throughout the body, tagging it biochemically in such a way that the liver or kidneys could clear it.

“Alzheimer’s disease is clearly a disease of the brain, but we need to pay attention to the whole body to understand where it comes from, and how to stop it,” he says

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داریوش طاهری

اولیــــــن نیستیــم ولی امیـــــد اســــت بهتـــرین باشیـــــم...! خدایــــــــــا نام و آوازه مـــن را چنان در حافظه‌ها تثبیت کن که آلزایمـــــــــــــر نیز توان به یغما بردن آن را نداشته باشد...!

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