First drug that targets 'traffic controller' cells in the brain could be a breakthrough in slowing progression of dementia, scientists say

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A team of scientists have developed a potentially breakthrough dementia drug that could prolong the life of brain cells — and could mark a new frontier of treatment for the disease.

Scientists from Ontario, Stanford University and the University of California found a twice-daily pill could reduce levels of a harmful brain protein called amyloid — one of the main hallmarks of the disease — by nearly 10 percent.

The experts say the benefits in patients' brains were observed after just six months on the medicine, as opposed to years like other experimental treatments.

Additionally, side effects were few and mild, with the most common being diarrhea and headaches.

Other novel dementia therapies in development, like donanemab, have raised concerns among experts due to known risks of brain bleeds, which have killed several trial patients.

The new drug, called LM11A-31, targets a specific receptor called P75NTR in the brain that helps regulate brain cell survival and development.

When cells, or neurons, die, messages can't be passed throughout the brain as effectively, which scientists believe is what causes the thinking and memory difficulties in dementia.

The results of a recent trial, published earlier this month in the journal Nature Medicine, found LM11A-31 enhanced the passage of signals between the receptor and cells to promote growth and survival.

The drug is the first to study a therapy that targets P75NTR, and was observed to significantly slow the build up of amyloid, a hallmark protein of Alzheimer's in patients' brains.

Researchers said the drug is 'exciting' because it directly improves the ability of brain neurons to survive.

Alzheimer's disease is the most common form of dementia and affects 6.7million Americans. With the aging population booming in the US, that number is expected to grow to 13million by 2050.

While the main cause of Alzheimer's disease is still debated, scientists believe the damage is likely to be the result of abnormal build-up of proteins — amyloid and tau — in and around brain cells.

In Alzheimer's patients, amyloid proteins are not effectively cleared from the body and eventually form plaques in the brain. Tau proteins detach from neurons to form tangles.

Both of these can lead to neuron death, which makes it difficult to deliver signals throughout the brain.

The Canadian and California researchers studied LM11A-31 in 242 participants with a confirmed mild-to-moderate Alzheimer's diagnosis over a 26-week period.

They took samples of cerebrospinal fluid (CSF) from the study participants to measure the level of amyloids present. CSF is a fluid that surrounds and protects the brain and spine.

In people receiving the twice-daily pill, the average buildup of amyloid was up to nine percent less than in the CSF of people receiving the drug.

The study said: 'Overall, these findings indicate that longitudinal AD-related increases in [CSF amyloids] were slowed or reversed by LM11A-31.'

The above graph shows the estimated projection of Alzheimer's disease patients in the US through 2060.

When measuring long-term changes in tau levels in CSF between the two groups, researchers did not find any significant differences.

The researchers acknowledged the limitations of the study, which included a limited time frame and a small participant pool. Therefore they were limited in their ability to assess any difference in cognitive changes.

Nonetheless, the researchers said the results of their study are promising because such significant findings are not typically seen in studies so early on, with most research taking two or more years to yield such results.

Co-author of the study Hayley Shanks, a neuroscience Ph.D. student at the University of Western Ontario, said: 'The reason this drug is exciting is because it's directly affecting the ability of the neurons to survive. It promotes their overall integrity, their branching and their synapses [where cells connect and communicate with each other].

'In [preliminary] animal models, it was shown that the drug was preserving these neurons or reversing the damage which translated to behavioral improvements, almost reverting the neurons back to a healthy state.'

Co-author Taylor Schmitz, a professor in the school of medicine at the University of Western Ontario, added: 'The drug slowed down the increase of this inflammation marker in the cerebrospinal fluid.

'This is significant because, in the past five years, inflammation has become a key factor in understanding Alzheimer's disease.'

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There is currently no cure for Alzheimer's and new drugs in development like donanemab only marginally slow the rate of progression and come with dangerous side effects like brain bleeding.

While the drug was hailed early on as a potential therapy, one-quarter of patients in the trial suffered brain swelling and three people died from brain swelling or bleeding that was attributed to the drug.

Another drug, Leqembi, works similarly to donanemab, but can also cause amyloid-related imaging abnormalities (ARIA), which are brain changes that can include bleeding and swelling.

It is FDA-approved but studies show about 20 percent of people who take the drug develop ARIA, but only 20 percent of those people experience symptoms.

For decades, researchers have focused on developing drugs that target the amyloids clumps - a hallmark sign of the dementia.

However, they have recently turned their focus to how tau proteins play a role in cognitive decline and there are currently at least six clinical trials either completed or in progress testing the safety and efficacy of vaccines to treat and prevent Alzheimer's disease via targeting both tau and amyloids.