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New vaccine could reduce or prevent impact of Alzheimer’s

“Alzheimer’s disease now accounts for 50 percent to 70 percent of dementia patients worldwide."

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The brain has about 100 billion cells called neurons.

By Stephen Beech via SWNS

A new vaccine could reduce or even prevent the devastating impact of Alzheimer’s disease, according to new research.

The jab, which targets a protein involved in the most common cause of dementia, helped eliminate toxic cells in mice with the condition.

Scientists say the mice had fewer amyloid plaques and less inflammation in their brain tissue after the SAGP vaccination - and they also showed improvement in behavior and awareness.

Researchers hope the vaccine that targets inflamed brain cells associated with Alzheimer’s offers fresh hope in treating soaring dementia cases.

More than 800,000 people are estimated to have dementia in the UK while around 3.7 million Americans had Alzheimer’s disease in 2017, according to the American Heart Association. That number is forecast to rise to 9.3 million by 2060.

The new vaccine has been developed by researchers at Juntendo University Graduate School of Medicine in Japan.

Bu it has yet to be tested in humans.

Study lead author Dr. Chieh-Lun Hsiao said: “Alzheimer’s disease now accounts for 50 percent to 70 percent of dementia patients worldwide.

"Our study’s novel 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.

“If the vaccine could prove to be successful in humans, it would be a big step forward towards delaying disease progression or even prevention of this disease.”

(Photo by Robina Weermeijer via Unsplash)

The researchers created an Alzheimer’s disease mouse model that mimics a human brain and simulates amyloid-beta-induced Alzheimer’s disease pathology.

Usually, people in the late stage of Alzheimer’s lack anxiety, which means they are not aware of the things around them.

Dr. Hsiao said the mice who received the vaccine had anxiety, which means that they were more cautious and more aware of things around them – a sign the researchers say could indicate a lessening of the disease. Several inflammatory biomarkers of Alzheimer’s disease were also reduced.

A behavior test on the mice at six months old also revealed that those that received the SAGP vaccine responded "significantly better" to their environment than those who received a placebo vaccine.

The SAGP-vaccinated mice tended to behave like normal healthy mice and exhibited more awareness of their surroundings.

The SAGP protein was shown to be located very near to specialized brain cells called microglia, which play a role in the immune defence of the central nervous system.

Dr. Hsiao explained that microglia help clear damaging plaque formed by proteins; however, they also trigger brain inflammation that can damage neurons and worsen cognitive decline in a person, which could be one of the causes of Alzheimer’s disease development.

(Photo by Steven HWG via Unsplash)

In Alzheimer’s disease, an accumulation of brain proteins called amyloid beta peptides clump together forming plaques that collect between neurons and disrupt cell function.

Dr. Hsiao said: “Earlier 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 behaviour of these mice for the better."

The research team say that previous studies suggest that the SAGP protein is "highly elevated" in microglia, which means that microglia are very important cells to target in Alzheimer’s disease.

Dr. Hsiao added: “By removing microglia that are in the activation state, the inflammation in the brain may also be controlled.

"A vaccine could target activated microglia and remove these toxic cells, ultimately repairing the deficits in behavior suffered in Alzheimer’s disease.”

The findings of the preliminary research were presented at the American Heart Association’s Basic Cardiovascular Sciences Scientific Sessions in Boston, Mass.

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