Experts observed in real time how a toxic Alzheimer's protein affects neural connections.
A team from the University of Edinburgh, in collaboration
with the Royal Infirmary, has achieved an unprecedented breakthrough: using living human brain
tissue to reproduce the early
development of Alzheimer's
in the laboratory.
The experiment allowed real-time observation of how a toxic protein characteristic of the disease damages the connections between neurons. This finding could accelerate the development of more effective treatments for the most common form of dementia, which affects more than 55 million people worldwide.
Scientists obtained fragments of healthy brain tissue during routine surgeries on cancer patients, with explicit consent, as reported by The Guardian.
The procedures were performed at the Royal Infirmary of
Edinburgh, and the material was
immediately preserved in bottles filled with oxygenated artificial
cerebrospinal fluid.
As soon as the procedures were completed, a team of researchers rushed in taxis to the laboratory, located just minutes away, to preserve the samples' viability.
"We practically ran back to the lab," Dr. Claire Durrant, study leader and researcher at Race Against Dementia, told The Guardian.
There, the fragments were cut into thin slices—less than a third of a millimeter—and placed on plates with nutrients in an incubator at 37°C, human body temperature.
Simulating Alzheimer's in Real Time
The researchers added a toxic form of the beta-amyloid protein, extracted from patients who had died from Alzheimer's, to the living tissue. This substance is directly implicated in the brain deterioration associated with the disease.
Compared to harmless versions of the same protein, tissue exposed to the toxic compound showed clear destruction of synapses—the connections that allow communication between neurons.
“We tried to mimic Alzheimer's disease,” Durrant explained to The Guardian. The effects were immediate. The neurons didn't attempt to repair the damage, as was the case with other forms of beta amyloid.
The study confirmed that even subtle changes in the natural levels of this protein are enough to alter cellular behavior.
Each human brain fragment was kept alive for up to 15 days, allowing for multiple consecutive observations and experiments with unprecedented fidelity to the behavior of a living human brain.
Key Discoveries About
Proteins and Brain Damage
One of the most revealing observations occurred in the temporal lobe, a region particularly vulnerable in the early stages of Alzheimer's.
Samples taken from that area released significantly higher levels of the tau protein, another of the disease's signature compounds. This release may be a pathway for cell spread, which would explain why the temporal lobe suffers early and accelerated damage.
"We believe this tool could help accelerate the translation of laboratory findings to patients," Durrant told the British media. His team suggested that the brain needs a precise balance of beta amyloid to function properly. Both excess and deficiency can trigger alterations.
A Step Toward New Therapies
This innovative study method could transform drug research. “It allows researchers to better examine Alzheimer's disease in real human brain cells, rather than relying on animal surrogates, such as mice,” said James Dyson, whose foundation contributed £1 million (more than $1.3 million) to the project.
By allowing the study of real synapses in real time, the technique could be used to develop and test drugs with greater precision.
According to a statement from Race Against Dementia, founder and former racing driver Sir Jackie Stewart stated, “Every three seconds someone develops dementia.” He made the decision to start the company after his wife was diagnosed with dementia.
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