Is this the beginning of the end for Alzheimer’s? Experimental vaccine prevents disease in early study

A new vaccine that appears to stop Alzheimer’s in its tracks is raising optimism that this may be the beginning of the end for the disease.

A study of the jab in mice showed that the shot not only removed harmful amyloid plaque from the brain, it also prevented the behavioral changes that normally plague Alzheimer’s patients.

It comes after a year in which two breakthrough drugs proved they could slow the disease, ending decades of failed trials and false hope. However, these treatments only give patients a few extra months of healthy life.

This vaccine could go even further in its ability to stop the disease — which affects at least 6 million Americans — from progressing before it reaches a point of no return, researchers say.

Dr. Chieh-Lun Hsiao, a cardiovascular researcher at Japan’s Juntendo, said: ‘If the vaccine could be successful in humans, it would be a big step towards delaying disease progression or even preventing this disease.’

The new study – which is still ongoing – involves testing the vaccine in mice that had mutated versions of an amyloid precursor protein inserted into their genes.

Amyloid plaques are a hallmark of Alzheimer’s and are thought to accelerate the death of brain cells.

There is still some debate as to whether they cause the disease or are a symptom of it.

Some mice received a vaccine, while others received a placebo. The vaccine given to mice aged two and four months was designed to target a specific molecule on the brain’s outer membrane of damaged or ‘senescent’ cells.

That molecule is called senescence-associated glycoprotein (SAGP).

By identifying this specific location on a cell, scientists can more precisely target the cause of Alzheimer’s – in this case, the accumulation of toxic plaques – rather than just the symptoms such as cognitive decline.

When the vaccine was first inserted into the mice, it effectively trained their immune systems to recognize SAGP on the surface of damaged cells as a harmful foreign invader.

After the immune system managed to seek out the SAGP, it launched an attack against them and killed them.

The vaccine effectively reduced SAGP and amyloid deposits in the mouse brains in the region responsible for language processes, attention and problem solving.

It showed other positive effects that suggest it could work in humans. When placed in a maze-type device to test the vaccine’s effects on behavior, the mice that received the SAGP vaccine tended to behave like normal healthy mice and showed more awareness of their surroundings.

Dr. Hsiao said: ‘Alzheimer’s disease now accounts for 50% to 70% of dementia patients worldwide. Our study’s new vaccine test in mice points to a potential way to prevent or modify the disease. The future challenge will be to achieve similar results in humans.’

He added: ‘Previous studies using different vaccines to treat Alzheimer’s disease in mouse models have been successful in reducing amyloid plaque deposits and inflammatory factors, but what makes our study different is that our SAGP vaccine also changed these mus’ behavior for the better. .’

The Japanese team’s findings are still in their early stages, and human trials could take years. But the research has received support from the influential American Heart Association.

In healthy people, amyloid proteins are removed from the brain.

But in a brain affected by Alzheimer’s, the amyloid-beta protein deposits build up over time and form ‘sticky’ plaques in the brain.

When the build-up of amyloid in the brain reaches a tipping point, it leads to the formation of tangles of a protein called tau.

The formation of these tangles disrupts the normal function of brain cells by disrupting the transport of essential molecules such as neurotransmitters involved in intercellular communication and nutrients such as glucose and oxygen.

Research into the precise mechanisms that cause Alzheimer’s disease is ongoing and far from being settled. Some researchers believe that tau has a greater role to play than amyloid plaques in the development of the disease.

Over time, the build-up of plaques and tau tangles damages synapses in critical areas of the brain, such as the hippocampus, for example, which is essential for the formation of memories, as well as the Entorhinal Cortex, which relays sensory information from the outer cortex of the brain to the hippocampus.

This buildup also damages the parietal lobe of the brain, which is closely related to sensory perception, spatial awareness, and the ability to sustain attention.

Alzheimer’s disease is the most common form of dementia, accounting for 60 to 70 percent of all cases, according to the World Health Organization (WHO).

So far, 2023 has been a banner year for Alzheimer’s research, with the emergence of two of the most promising treatments in decades after years of failed trials and billions spent.

Last month, the Food and Drug Administration took the long-awaited step of approving a monoclonal antibody treatment for Alzheimer’s disease called Leqembi, which was found to slow the pace of cognitive decline by 27 percent in early-stage patients.

The historic approval of Leqembi was followed by promising trial results of another treatment from Eli Lilly called donanemab, which slowed disease progression by 35 percent.

Although the development of both treatments marks a major step forward in understanding the mechanisms by which Alzheimer’s robs a person of what it means to be themselves, they are not perfect.

Slow decline of 27 or even 35 percent really equates to only another four to eight months without extremely serious symptoms such as the inability to remember relatives’ names, incontinence or loss of fine motor skills.

However, a vaccine could stop Alzheimer’s in its tracks and even prevent the build-up of plaques that kill healthy brain cells to the point where they cannot communicate with each other, leading to problems with memory and reasoning.