Is this the beginning of the end for Alzheimer’s disease? Experimental Vaccine Prevents Disease In Early Study – Contributing To Dementia Year Breakthroughs So grab our interactive map to see how many people in YOUR county have a memory impairment

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

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

It comes after a year in which two groundbreaking drugs proved they could slow the disease, ending decades of failed trials and false hopes. 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 developing before it reaches a point of no return, researchers say.

Dr. Chieh-Lun Hsiao, a cardiovascular researcher at Juntendo in Japan, said: “If the vaccine could be successful in humans, it would be a big step towards slowing 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 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 two- and four-month-old mice, 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 spot on a cell, scientists can more precisely target the cause of Alzheimer’s disease — in this case, the buildup of toxic plaques — rather than just the symptoms such as cognitive decline.

Once introduced 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 was primed to detect SAGP, it attacked and killed them.

The vaccine effectively reduced SAGP and amyloid deposits in the mouse brain in the area 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-like device to test the vaccine’s impact on behavior, the mice given the SAGP vaccine tended to behave like normal, healthy mice and showed greater awareness of their surroundings.

Dr. Hsiao said: ‘Alzheimer’s disease now accounts for 50% to 70% of dementia patients worldwide. The new vaccine test from our study in mice points to a possible way to prevent or modify the disease. The challenge for the future 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 behavior of these mice changed for the better. .’

The Japanese team’s findings are still in the 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 brains suffering from Alzheimer’s disease, the deposits of the amyloid beta protein build up over time to form ‘sticky’ plaques in the brain.

When the buildup 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 functioning of brain cells by interfering with 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 complete. Some researchers believe that tau plays a bigger role than amyloid plaques in the progression of the disease.

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

That buildup also damages the parietal lobe of the brain, which is intimately involved in 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 peak year for Alzheimer’s research, with the arrival of two of the most promising treatments in decades after years of failed trials and billions of dollars spent.

Last month, the Food and Drug Administration took the long-awaited step to approve a monoclonal antibody treatment for Alzheimer’s called Leqembi.

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

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

A delayed decline of 27 or even 35 percent really only adds up to an extra four to eight months without extremely serious symptoms such as the inability to remember the names of loved ones, incontinence or a loss of fine motor skills.

However, a vaccine could stop Alzheimer’s and even prevent the buildup of plaques that kill healthy brain cells to the point where they can no longer communicate with each other, leading to memory and reasoning problems.