New Alzheimer’s drug may slow cognitive decline

New Alzheimer’s drug may slow cognitive decline

2023-05-10 21:00:12

For the first time, researchers have described the structure of a special type of amyloid beta plaque protein. associated with the progression of Alzheimer’s disease (EA).

In a study, published in the magazine ‘Neuron’scientists have shown that small aggregates of the amyloid beta protein could float through brain tissue fluidreach many regions of the brain and alter the functioning of local neurons. The research also provides evidence that a recently approved AD treatment could neutralize these small diffusible aggregates.

Alzheimer’s, one of the causes of dementia, affects more than 50 million people worldwide. Previous research has found that AD patients have an abnormal accumulation of a natural substance –the amyloid beta protein– in the brain that can alter neurotransmission. Currently, the disease has no cure. But in recent years, scientists have developed new treatments that may reduce AD ​​symptomssuch as memory loss.

Slow down cognitive decline

“The article is very timely because, for the first time in human historywe have an agent capable of treating Alzheimer’s patients in such a way that slow down their cognitive decline –says Dennis Selkoe, author of the article at Brigham and Women’s Hospital in Boston (United States)–. And we’ve never been able to say those words until the last few months.”

In January, the US Food and Drug Administration approved lecanemab, an antibody therapy from Lilly to treat AD. In a phase III clinical trial, lecanemab slowed cognitive decline in patients with early AD.

Scientists suspect that the positive effect of the drug may be associated to your ability to bind and neutralize soluble aggregates of amyloid beta protein, also known as protofibrils or oligomers, which are small, free-floating clumps of amyloid beta protein.

These small clumps can form in the brain before further aggregating and becoming large amyloid plaques. Small aggregates too can break off and spread from amyloid plaques already existing.

“But no one has been able to define with structural rigor what a ‘protofibril’ or ‘oligomer’ is that lecanemab binds to,” said Andrew Stern, a neurologist at Brigham and Women’s Hospital and first author of the study. “Our paper identifies that structure after isolating it from the human brain.This is important because patients and drug manufacturers they’ll want to know what exactly the lecanemab binds to. Could you reveal something special about how it works?” he wonders.

Stern, Selkoe and their team managed to isolate floating beta-amyloid aggregates by immersing postmortem brain tissues from typical AD patients in saline solutions, which were then spun at high speed.

Key to future drugs

These tiny aggregates of amyloid beta protein access important brain structures As the hippocampus, which plays a key role in memory. In collaboration with colleagues from the Cambridge Laboratory of Molecular Biology (UK), they determined the atomic structure of these tiny aggregates, down to the individual atom.

“If you don’t know your enemies, it’s hard to beat them,” Selkoe exemplifies. “It was a very nice coincidence that all this work we were doing coincided with the time when the lecanemab became widely known and available. This investigation brings together the identity of the bad guy and something that can neutralize him.”

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Next, the team plans to observe how these tiny amyloid beta aggregates travel through the brains of living animals and study how the immune system responds to these toxic substances. Recent research has shown that the brain’s immune system’s reaction to amyloid beta is a key component of AD.

“If we can to find out exactly how these tiny diffusible fibrils exert their toxicitymaybe the next AD drugs could be better,” says Stern.

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