MIT scientists find new way to reverse Alzheimer’s after trial participant dies from previous drug

Scientists at the Massachusetts Institute of Technology (MIT) have discovered a new way to reverse Alzheimer’s disease – a major breakthrough with ‘dramatic’ results.

The researchers used a peptide, or series of amino acids, to interfere with an enzyme that is typically overactive in the brains of people with the disease.

The chemical compound prevents an enzyme, called CDK15, in the brain linked to Alzheimer’s disease from becoming overactive and damaging neurons, causing cognitive decline.

Researchers hope their findings can serve as the center of future research into a drug that could reverse the devastating effect of the disease.

It’s also because lecanemab, a recently approved Alzheimer’s treatment considered a game-changer for its ability to slow cognitive decline, was linked to the death of a 79-year-old Florida woman.

A doctor viewing MRI brain scans of Alzheimer’s patients. Scientists at MIT discovered a treatment with ‘dramatic’ results

Li-Huei Tsai, senior author of the study from MIT, said: ‘We found that the effect of this peptide is simply remarkable. We saw amazing effects in terms of reducing neurodegeneration and neuroinflammatory responses, and even saving behavioral disorders.’

After further experiments, the researchers are optimistic that the peptide could eventually be used to treat patients with Alzheimer’s and other dementias.

The study, published in the PNASshowed that when the scientists tested the peptide on mice with Alzheimer’s disease that had hyperactive CDK5, there was less DNA damage, neural inflammation and neuron loss.

They were compared to a control group of mice that received an encoded version of the peptide.

The researchers also tested the peptide in mice with Alzheimer’s disease that have a mutated Tau protein form that leads to brain protein tangles.

After treatment, the mice had less Tau prevalence and neuron loss.

There were also behavioral benefits: The mice given the peptide performed better at tasks involving navigating a water maze than mice given the control peptide.

The scans above show the woman’s brain before treatment with the antibody (left) and after (right). Her brain became swollen during treatment and showed signs of bleeding

Meanwhile, the brains of a third patient who died while being treated with an experimental Alzheimer’s drug, which doctors hoped would mark the “beginning of the end” for the condition, have been examined.

The autopsy of the unnamed 79-year-old Florida woman “strongly suggests that lecanemab infusions were a catalyst leading to the events that resulted in her death,” said Vanderbilt University pathologist Hannah Harmsen, Science reported.

The patient was in the extension phase of the Phase 3 trials for the antibody drug lecanemab, supported by biotech company Eisai. The treatment works by removing amyloid beta proteins from the brain, which are thought to cause Alzheimer’s disease.

The woman suffered extensive swelling and bleeding in the brain after treatment for more than 18 months.

She was hospitalized with seizures in mid-September 2022 and died five days later.

As with all Alzheimer’s patients, the woman was at risk for cerebral amyloid angiopathy (CAA).

Alzheimer’s disease causes beta-amyloid protein to build up around brain cells and form deposits known as plaques.

In half of the patients, the protein replaces the muscles in the walls of blood vessels, making them weak.

Antibodies, including lecanemab, eliminate the amyloid, leaving the blood vessels vulnerable and at risk of serious bleeding.

Brian imaging is used to find signs of CAA, and an autopsy can only make a definitive diagnosis.

The Florida woman’s case report showed strong evidence of CAA – multiple cerebral hemorrhages and blood vessel degeneration.

Lecanemab is one of several experimental Alzheimer’s drugs that target amyloid beta proteins, which accumulate in the brains of people with the disease.

Many scientists claim that this buildup is responsible for the disease, although protein deposits are also seen in the brains of healthy people.

The amyloid-seeking antibodies help clear the proteins, but can cause brain swelling and bleeding in the process.

This is a condition medically called amyloid-related imaging abnormalities (ARIA) because it is diagnosed through brain scans.

Finding a cure for Alzheimer’s disease – or at least drugs that can prevent or slow it down – has been the priority of neuroscientists around the world in recent years.

The disease affects 6 million Americans, and the figure is expected to double by 2030 as conditions that cause the disease, such as obesity, become more common and lifespan increases.

It almost always strikes in old age, with few cases among people under 60 years of age.