Is this the beginning of the end for Alzheimer’s? Experimental vaccine prevents disease in early study – adding to year of dementia breakthroughs. So take our interactive map to see how many have memory-robbing disorder in YOUR county

A new vaccine that appears to stop Alzheimer’s adds to optimism that this could be the beginning of the end for the disease.

A study of the injection in mice found that the injection not only cleared harmful amyloid plaque from the brain, but also prevented behavioral changes that normally plague Alzheimer’s sufferers.

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

This vaccine could go even further in its ability to prevent the disease, which affects at least 6 million Americans, from progressing before it reaches a point of no return, the 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 in slowing the progression of the disease or even preventing it.”

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 disease and are believed 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 at two and four months of age 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 pinpointing this specific site on a cell, scientists can more precisely target the root cause of Alzheimer’s—in this case, the buildup of toxic plaques—rather than just symptoms like cognitive decline.

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

After the immune system got ready to look for SAGP, it mounted an attack on them, killing them.

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

It showed other positive effects that suggest it might work in humans. When placed in a maze-like device to test the impact of the vaccine 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 50-70% of dementia patients worldwide. The new vaccine test from our mouse study points to a potential way to prevent or modify the disease. The future challenge will be to achieve similar results in humans.”

From 1906, when clinical psychiatrist Alois Alzheimer first reported a “serious disease of the cerebral cortex,” to discovering the mechanics of the disease in the 1980s and 1990s, to today’s “breakthrough” drug lecanemab, scientists they have spent more than a century trying to deal with the brutal disease that robs people of their cognition and independence

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, however what makes our study different is that our SAGP vaccine also altered the behavior of these mice 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 endorsement from the influential American Heart Association.

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

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

When amyloid buildup 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 functioning of brain cells by interrupting the transport of essential molecules such as neurotransmitters involved in intercellular communication and nutrients such as glucose and oxygen.

Research into the exact mechanisms that cause Alzheimer’s disease is ongoing and far from settled. Some researchers believe that tau has a more important role than amyloid plaques in the progression of the disease.

Over time, the buildup of tau plaques and tangles damages synapses in critical regions of the brain, such as the hippocampus, for example, which is crucial for memory formation, as well as the entorhinal cortex, which relays sensory information from the cortex. outside of the brain. to the hippocampus

That buildup also damages the parietal lobe of the brain closely involved with 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 advent of two of the most promising treatments in decades after years of failed trials and billions spent.

Last month, the Food and Drug Administration (FDA) took the long-awaited step of approving a monoclonal antibody treatment for Alzheimer’s disease called Leqembi, which has been shown to slow the rate of cognitive decline by 27 percent in early-stage patients.

Leqembi’s landmark approval was followed by promising trial results from another Eli Lilly treatment called donanemab that slowed disease progression by 35 percent.

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

Decreasing the decline by 27 or even 35 percent really only equates to an additional four to eight months without extremely severe symptoms, such as an inability to remember the names of loved ones, incontinence, or loss of function. fine motor.

However, a vaccine could stop Alzheimer’s in its tracks and even prevent the buildup of plaques that destroy healthy brain cells to the point where they can’t communicate with each other, leading to problems with memory and reasoning.