Repairing the Blood Brain Barrier Reversed Alzheimer’s Disease in Mice, a Hopeful Result for Humans
Alzheimer’s disease can, in simple terms, be considered as an accumulation of waste in the brain which disrupts neural activity. This accumulation leads to the loss of neural connections and the integrity of the brain, resulting in familiar symptoms such as severe memory loss and emotional deregulation.
As research on origins, treatment and prevention of disease is progressing, scientists explore new ways to improve brain ability to eliminate toxic debris that accumulate in Alzheimer’s disease.
In a new study, a team from the Institute for Bio-Engineering in Catalonia (IBEC), the Western China Hospital of the University of Sichuan (WCHSU) and colleagues from the United Kingdom have considerably reversed Alzheimer’s disease in mice by improving the vascular waste waste system using bioactive nanoparticles.
Their results, published in nature Signal transduction and targeted therapyOpen the way for better treatment options for Alzheimer’s disease in humans.
Alzheimer’s is a waste elimination problem
Our brains are not only protected by the skull, but also by a delicate and semi-permeable membrane called blood-brain barrier (BBB). This barrier creates a stable environment to support critical neural functions, acting as a goalkeeper between the hair network of the brain, nourishing each neuron and the broader vascular system of the body. It protects the brain from toxins and pathogens, regulates the passage of essential nutrients and expels harmful compounds which accumulate naturally during normal metabolism.
One of these compounds is the beta amyloid (Aβ), a key contributor to Alzheimer’s disease. Although everyone produces Aβ throughout life, its accumulation in plates increases with age. When the capacity of the BBB to erase Aβ decreases, its toxic concentration increases, triggering the characteristic of Alzheimer’s neurodegenerative cascade.
Previous research has identified several molecular components involved in this clearance process, including protein 1 linked to lipoprotein receptors (LRP1). This molecule maintains the integrity of the BBB and helps to erase Aβ, but when its function is altered, Aβ accumulates at dangerous levels.
Based on this insight, the team designed a nanoparticle which imitates LRP1, allowing it to “transport” Aβ through the BBB in the blood circulation, where it can be removed safely.
Learn more: The blood test of Alzheimer’s disease could lead to more efficient and more efficient treatment
Nanoparticles reduced the 50% amyloid beta version
To test therapy, researchers injected three doses of nanoparticles into genetically modified mice to overcome Aβ, leading to a cognitive decline similar to Alzheimer in humans.
“Only an hour after injection, we observed a reduction of 50 to 60% in quantity Aβ inside the brain,” explained the first author of the Junyang Chen study, researcher at West China hospital at the University of Sichuan and PH.D. Student at University College London (UCL) in a press release.
To assess the long -term effects of treatment, the team has monitored the behavior and mouse memory capacity over several months. The results were striking: an 18 -month -old mouse – equivalent to a 90 -year -old human – returned to the behavior of a healthy mouse after receiving the treatment of nanoparticles six months earlier.
“What is remarkable is that our nanoparticles act as a medication and seem to activate a feedback mechanism which brings this clearance route to normal levels,” said Giuseppe Battaglia, professor at Ibec and study chief in the version.
Use of biophysics to advance the search for Alzheimer’s
“The long -term effect comes from the restoration of the vascular system of the brain. We think it works like a cascade: when toxic species such as Aβ accumulate, the disease progresses. But once the vascular system is capable of operating again, it begins to eliminate Aβ and other harmful molecules, allowing the whole system to recover its balance, “added Aβ and other harmful molecules, which allows the whole system to recover its balance,” added batellers.
The new drug acts as a molecular “switch”, restarting the brain waste management system by imitating the properties of LRP1. It has the rare capacity to cross the BBB, to bond in Aβ and to transport it, to restore the role of the vascular system as a “highway” of brain waste. This process supports the restoration of a healthy neural function.
“Our study has shown remarkable efficiency to obtain a rapid clearance of Aβ, restoring a healthy function in the blood barrier and leading to a striking reversal of Alzheimer’s pathology,” said the co-author of the study, Lorena Ruiz Perez, researcher at IBEC.
Given the devastating impact of this neurodegenerative condition, this innovative therapeutic approach could one day improve the treatment of Alzheimer’s in humans by combining biophysical principles with our growing understanding of brain physiology.
Learn more: Lower alzheimer risk with the mental diet
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