First drug to target ‘traffic controller’ cells in the brain could be a breakthrough in slowing the progression of dementia, scientists say

A team of scientists has developed a potentially groundbreaking dementia drug that could extend the lifespan of brain cells – and mark a new frontier in treating the disease.

Scientists from Ontario, Stanford University and the University of California found that a twice-daily pill can reduce the amount of a harmful brain protein called amyloid – one of the key hallmarks of the disease – by almost 10 percent.

The experts say the benefits were seen in patients’ brains after just six months of taking the drug, as opposed to years as with other experimental treatments.

Furthermore, side effects were minor and mild, with diarrhea and headache being the most common.

Other new dementia therapies in development, such as donanemab, have raised concerns among experts due to the known risks of brain hemorrhage, which has killed several trial patients.

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

When cells or neurons die, messages cannot be passed through the brain as effectively, which scientists believe is the cause of the thinking and memory problems in dementia.

The Results A recent study published earlier this month in the journal Nature Medicine found that LM11A-31 improved 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 buildup of amyloid, a hallmark protein of Alzheimer’s disease, 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, affecting 6.7 million Americans. With the aging population exploding in the US, this number is expected to increase to 13 million by 2050.

Although the main cause of Alzheimer’s disease is still debated, scientists think the damage likely results from an abnormal buildup of proteins – amyloid and tau – in and around brain cells.

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

Both can lead to neuron death, making it difficult to send signals through the brain.

The Canadian and Californian researchers studied LM11A-31 in 242 participants with a confirmed mild to moderate diagnosis of Alzheimer’s over a period of 26 weeks.

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

In people given the twice-daily pill, the average build-up of amyloid was up to nine percent less than in the cerebrospinal fluid of people given 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 cerebrospinal fluid between the two groups, the researchers found no 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.

Nevertheless, the researchers said the results of their study are promising because such significant findings are not typically seen this early in studies, with most studies taking two or more years to produce such results.

Co-author of the study Hayley Shanks, a neuroscientist Ph.D. student at the University of Western Ontario, said: ‘The reason this drug is so exciting is because it directly affects the neurons’ ability to survive. It promotes their overall integrity, their branches and their synapses (where cells connect and communicate with each other).

‘In (preliminary) animal models, the drug was shown to preserve these neurons or reverse the damage, which translated into behavioral improvements, almost returning the neurons to healthy condition.’

Co-author Taylor Schmitz, professor of medicine at the University of Western Ontario, added: ‘The drug slowed the increase in this inflammatory marker in the cerebrospinal fluid.

‘This is important because inflammation has become a key factor in understanding Alzheimer’s disease over the past five years.’

There is currently no cure for Alzheimer’s disease and new drugs in development, such as donanemab, only marginally slow progression and carry dangerous side effects such as brain haemorrhage.

Although the drug was early touted as a potential therapy, a quarter of patients in the study experienced brain swelling and three people died from brain swelling or bleeding attributed to the drug.

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

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

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

However, they have recently shifted their focus to how tau proteins play a role in cognitive decline and at least six clinical trials are currently completed or underway to test the safety and efficacy of vaccines to treat and prevent Alzheimer’s disease. prevention by targeting both tau and Alzheimer’s disease. amyloids.