Hydrangea compound inhibits buildup of Alzheimer’s-associated protein

A new study has found that a substance extracted from the leaves of the hydrangea plant could be an effective treatment against the protein plaques that are thought to contribute to the development of Alzheimer’s disease.

Much recent research has concentrated on developing treatments to slow or reverse Alzheimer’s disease (AD). With studies suggesting a link between brain plaques caused by the aggregation of amyloid beta protein and cognitive decline, many potential treatments have focused on addressing this particular brain pathology.

Now, researchers from Sahmyook University, South Korea, have found that a naturally occurring substance found in hydrangea leaves shows great promise in treating the amyloid beta plaques thought to contribute to AD.

The substance in question is phyllodulcin, found in the Hydrangea macrophylla. Dried hydrangea leaves are commonly used in Asian countries to make medicinal tea, and phyllodulcin is known for being a potent natural sweetener, 400 to 800 times sweeter than sucrose. In addition, recent studies have shown that phyllodulcin can cross the blood-brain barrier and may inhibit amyloid beta protein aggregation in the brain.

“We focused on increasing the level of evidence regarding phyllodulcin by using various experimental techniques,” said Se Jin Jeon, one of the study’s co-authors. “We hypothesized that phyllodulcin may enter the brain and inhibit amyloid beta aggregation, resulting in the improvement of various brain lesions appearing in AD.”

To test their hypothesis, the researchers used mice that had been genetically modified to develop amyloid plaques that model AD. They gave the mice phyllodulcin or a control substance orally once every three days for a month. After that, they tested the animals’ learning and memory before their brain tissue was analyzed.

They found that phyllodulcin inhibited amyloid beta aggregation and broke down existing aggregations. They also found that the extract reduced amyloid beta-related neurotoxicity and alleviated memory impairment, which the researchers attributed to a reduction in aggregates.

“Our study is the first to report that phyllodulcin can modify the underlying pathogenesis of Alzheimer’s disease, suggesting the possibility of preventing dementia or delaying the progression of the disease,” Jeon said.

The researchers hope their study will lead to the development of phyllodulcin-based compounds to treat AD.

“It will take more than 20 years to develop a treatment, but at this stage, the results of this study can be used to provide a guide map that can help prevent or improve dementia symptoms,” said Jeon.

The study was published in the journal Biomedicine & Pharmacotherapy.

Source: Sahmyook University

A new study has found that a substance extracted from the leaves of the hydrangea plant could be an effective treatment against the protein plaques that are thought to contribute to the development of Alzheimer’s disease.

Much recent research has concentrated on developing treatments to slow or reverse Alzheimer’s disease (AD). With studies suggesting a link between brain plaques caused by the aggregation of amyloid beta protein and cognitive decline, many potential treatments have focused on addressing this particular brain pathology.

Now, researchers from Sahmyook University, South Korea, have found that a naturally occurring substance found in hydrangea leaves shows great promise in treating the amyloid beta plaques thought to contribute to AD.

The substance in question is phyllodulcin, found in the Hydrangea macrophylla. Dried hydrangea leaves are commonly used in Asian countries to make medicinal tea, and phyllodulcin is known for being a potent natural sweetener, 400 to 800 times sweeter than sucrose. In addition, recent studies have shown that phyllodulcin can cross the blood-brain barrier and may inhibit amyloid beta protein aggregation in the brain.

“We focused on increasing the level of evidence regarding phyllodulcin by using various experimental techniques,” said Se Jin Jeon, one of the study’s co-authors. “We hypothesized that phyllodulcin may enter the brain and inhibit amyloid beta aggregation, resulting in the improvement of various brain lesions appearing in AD.”

To test their hypothesis, the researchers used mice that had been genetically modified to develop amyloid plaques that model AD. They gave the mice phyllodulcin or a control substance orally once every three days for a month. After that, they tested the animals’ learning and memory before their brain tissue was analyzed.

They found that phyllodulcin inhibited amyloid beta aggregation and broke down existing aggregations. They also found that the extract reduced amyloid beta-related neurotoxicity and alleviated memory impairment, which the researchers attributed to a reduction in aggregates.

“Our study is the first to report that phyllodulcin can modify the underlying pathogenesis of Alzheimer’s disease, suggesting the possibility of preventing dementia or delaying the progression of the disease,” Jeon said.

The researchers hope their study will lead to the development of phyllodulcin-based compounds to treat AD.

“It will take more than 20 years to develop a treatment, but at this stage, the results of this study can be used to provide a guide map that can help prevent or improve dementia symptoms,” said Jeon.

The study was published in the journal Biomedicine & Pharmacotherapy.

Source: Sahmyook University