A new way to reverse Alzheimer’s has been discovered by scientists at the Massachusetts Institute of Technology (MIT) — a major breakthrough with ‘dramatic’ results.
The researchers used a peptide, or string of amino acids, to interfere with an enzyme that is typically overactive in the brains of people with the disease.
The chemical compound stops an enzyme, called CDK15, in the brain linked to Alzheimer’s from becoming overactivated and harming neurons — causing cognitive decline.
Researchers hope their findings could serve as the center of future research into a drug that can reverse the disease’s devastating effect.
It also comes as lecanemab, a recently approved Alzheimer’s treatment deemed a game-changer for its ability to slow cognitive decline, was linked to the death of a 79-year-old woman from Florida.
Brain scans of mice with Tau proteins stained purple. The left picture shows the prevalence of Tau proteins in neurons from mice treated with a scrambled version of the peptide, compared to mice treated with the new peptide showing far less Tau proteins
A doctor looking at MRI brain scans of Alzheimer’s patients. Scientists at the MIT discovered a treatment with ‘dramatic’ results
Li-Huei Tsai, the study’s senior author from MIT, said: ‘We found that the effect of this peptide is just remarkable. We saw wonderful effects in terms of reducing neurodegeneration and neuroinflammatory responses, and even rescuing behavior deficits.’
After further experiments, the researchers are optimistic that the peptide could ultimately be used to treat patients with Alzheimer’s and other types of dementia.
The study, published in the PNAS, showed that when the scientists tested the peptide on mice with Alzheimer’s disease who had a hyperactive CDK5, there was less DNA damage, neural inflammation and neuron loss.
They were compared to a control group of mice given a scrambled version of the peptide.
The researchers also tested the peptide in mice with Alzheimer’s who have a mutant Tau protein form that leads to brain protein tangles.
After treatment, the mice had fewer Tau prevalence and neuron loss.
There were also behavioral benefits: the mice who received the peptide were better at tasks where they had to navigate a water maze than mice given the control peptide.
The above scans show the woman’s brain before treatment with the antibody (left) and afterwards (right). Her brain became swollen during the treatment and showed signs of bleeding
Meanwhile, a third patient who died while being treated with an experimental Alzheimer’s drug, that doctors hoped would herald the ‘beginning of the end’ for the condition has had their brain examined.
The autopsy of the unnamed 79-year-old woman from Florida ‘strongly suggests that lecanemab infusions were a catalyst leading to the events resulting in her death’, Vanderbilt University pathologist Hannah Harmsen said, Science reported.
The patient was in the extension phase of the phase 3 trials for the antibody drug lecanemab, backed by biotech company Eisai. The treatment works by clearing amyloid-beta proteins from the brain, which is thought to cause Alzheimer’s.
The woman suffered extensive swelling and bleeding in the brain after receiving the treatment for more than 18 months. She was admitted to the hospital with seizures in mid-September 2022 and died five days later.
As with all Alzheimer’s patients, the woman was at risk of cerebral amyloid angiopathy (CAA).
Alzheimer’s causes beta-amyloid protein to accumulate around brain cells, forming deposits known as plaques.
In half of the sufferers, the protein replaces muscle in blood vessel walls, leaving them weak.
Antibodies, including lecanemab, eliminate the amyloid, making the blood vessels fragile and at risk of serious bleeding.
Brian imaging is used to find signs of CAA, and an autopsy can only determine a definitive diagnosis.
The case report of the woman in Florida demonstrated strong evidence of CAA — multiple brain hemorrhages and the degeneration of blood vessels.
Lecanemab is one of several experimental Alzheimer’s drugs that target amyloid-beta proteins, which build up in the brains of people in the disease.
Many scientists argue this build-up is responsible for the disease, although protein deposits are also seen in the brains of healthy people.
The amyloid-seeking antibodies help to remove the proteins, but in the process, can cause brain swelling and bleeding.
This is a condition medically termed amyloid-related imaging abnormalities (ARIA) because it is diagnosed via brain scans.
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