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In mice, the antibody removes amyloid and improves vascular function without increasing the risk of cerebral hemorrhage-ScienceDaily




As people grow older, normal brain proteins known as amyloid beta often begin to collect in the harmful amyloid plaques of the brain. Such plaques can be the first step on the road to Alzheimer’s disease. When they form around blood vessels in the brain, a condition known as cerebral amyloid angiopathy, plaque also increases the risk of stroke.

Several antibodies that target amyloid plaques are being studied as experimental treatments for Alzheimer’s disease. Such antibodies have not yet been evaluated in clinical trials, but may also treat cerebral amyloid angiopathy. However, all anti-amyloid antibodies that successfully reduce amyloid plaques in Alzheimer’s disease clinical trials can also cause the nasty side effects of increased risk of brain swelling and bleeding.

Researchers at Washington University in St. Louis have now identified antibodies that remove amyloid plaques from brain tissue and blood vessels in mice without increasing the risk of cerebral hemorrhage. This antibody targets a trace component of amyloid plaques known as apolipoprotein E (APOE).

Survey results published on February 17 Scientific translation medicine, Suggests a potentially safer approach to the elimination of harmful amyloid plaques as a method of treating Alzheimer’s disease and cerebral amyloid angiopathy.

“Alzheimer’s disease researchers have been looking for treatments to reduce amyloid in the brain for decades, and now that there are some promising candidates, we know that this complication is present. “It was,” said senior author David Holtzmann, MD, Andrew B. and Professor Gretchen P. Jones, and Dean of the Department of Neurology. “Each antibody that removes amyloid plaques in clinical trials is a little different, but it has more or less this problem. Targeting APOE takes a different approach and seems to be effective in removing it. This potential Amyloid from both brain tissue and blood vessels, while avoiding dangerous side effects. “

A side effect called ARIA for amyloid-related imaging abnormalities can be confirmed by brain scanning. Such abnormalities indicate swelling and bleeding of the brain caused by inflammation, which can lead to headaches, confusion, and even seizures. In clinical trials of anti-amyloid antibodies, about 20% of participants develop ARIA, but not all have symptoms.

Anti-amyloid antibodies work by warning the immune system of the presence of unwanted substances (amyloid plaques) and instructing the cleanup crew (inflammatory cells known as microglia) to remove such debris. ARIA appears to be the result of an overly enthusiastic inflammatory response. Holtzmann and graduate student lead author Monica Zion found a more suppressed response in which antibodies that target only a small portion of amyloid plaques remove plaques from both brain tissue and blood vessels without causing ARIA. I suspected that it would induce it.

Fortunately, they had such antibodies at hand. It is an antibody called HAE-4 that is sparsely found in amyloid plaques and targets a specific form of human APOE that causes the removal of plaques from brain tissue. To determine if HAE-4 also removes amyloid from the cerebrovascular disease, researchers used mice genetically modified with the human genes for amyloid and APOE4. APOE4 is associated with an increased risk of developing Alzheimer’s disease and cerebral amyloid angiopathy. By about 6 months of age, these mice develop abundant amyloid plaques in brain tissues and blood vessels. In addition to Holtzmann and Zion, the research team includes co-author Dr. Hong Jiang, senior scientist in Holtzmann’s lab, Dr. Gregory J. Zipfell, and a prominent professor of neurosurgery, Ralph G. Dacy. The person responsible for neurosurgery was included. , Above all.

Experiments have shown that treatment of mice with HAE-4 for 8 weeks reduces amyloid plaques in brain tissue and cerebrovascular disease. Treatment has also significantly improved the ability of cerebrovascular to expand and contract on demand, an important sign of vascular health.

Cerebrovascular amyloid plaques are dangerous because they can lead to obstructions and ruptures that cause stroke. The researchers compared the number of cerebral hemorrhage in mice treated for 8 weeks with either HAE-4 or aducanumab, an anti-amyloid antibody in a phase 3 clinical trial of Alzheimer’s disease. Mice showed small baseline levels of cerebral hemorrhage due to a genetic predisposition to the accumulation of amyloid in blood vessels. However, aducanumab significantly increased the number of bleedings, but HAE-4 did not.

Further investigation revealed that HAE-4 and aducanumab initially elicited an immune response against amyloid plaques of similar intensity. However, mice treated with anti-APOE antibody resolved the inflammation within 2 months, whereas mice treated with anti-amyloid antibody persisted in inflammation.

“Some people develop cerebral amyloid angiopathy and not Alzheimer’s disease, but they can have a stroke instead,” Holtzmann said. “Amyloid accumulation in the cerebrovascular disease can be controlled by controlling blood pressure, etc., but there is no special treatment. This study not only shows that the condition can be treated with an animal model, but it is also exciting. However, it may be possible to do so without side effects that undermine the effectiveness of other anti-amyloid therapies. “


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