Alzheimer’s disease medication could treat obesity-induced heart disease, new study suggests

Drugs already tested in humans could be used to treat obesity-induced heart disease, saving about a decade of work, a Deakin University study has found.

New research has discovered Alzheimer's medications could be used to treat heart disease. Professor Sean McGee in the lab at Waurn Ponds campus. Picture: Supplied

Medications developed for Alzheimer’s disease could treat obesity-induced heart disease, new research suggests.

Researchers from Deakin University have discovered a link between obesity and amyloid beta – a protein previously implicated in Alzheimer’s disease development.

Obesity-induced heart disease affects up to 10 per cent of the population in certain age ranges, and is considered an untreatable condition, with 75 per cent of people not surviving more than five years beyond diagnosis.

Professor of Medical Biology at Deakin’s School of Medicine and the Institute for Mental and Physical Health and Clinical Translation (IMPACT) Sean McGee said amyloid beta accumulated in the brain, causing the deposition of brain plaques, and contributing to Alzheimer’s disease development.

Professor McGee said tests in the world-first study revealed amyloid beta was secreted from fat tissue into the bloodstream.

Researchers looked at both lean mice, and mice fed a high-fat diet resulting in obesity.

“It was clear that obese mice had much higher levels of amyloid beta in their blood,” he said.

“This led us to ask whether amyloid beta was a causative factor in heart disease, so we treated normal lean mice with amyloid beta and then followed their heart metabolism and function, and found that it induced cardiac disease – just like obesity.”

Professor McGee said the team observed amyloid beta collected in the mitochondria of the heart, and this accumulation prevented energy generation in heart cells.

He said this was enough to cause heart disease.

“To our knowledge, this is the first time that amyloid beta has been implicated in a disease that is not Alzheimer’s,” he said.

“To this point, it was thought that the negative effects of amyloid beta were restricted to the brain.”

The study results, published in Nature Communications this month, are the first to describe the production and release of amyloid beta by fat tissue as a cause of heart disease.

The discovery also identified a possible approach to treating obesity-related heart failure.

Professor McGee said some therapies and drugs developed for Alzheimer’s disease that could be used to treat obesity-induced heart disease.

“Many of these therapies were very effective in blocking the effects of amyloid beta and were safe in humans but most failed to effectively treat Alzheimer’s disease for various reasons,” he said.

“So we treated obese mice with one of these developmental Alzheimer’s disease drugs, and confirmed that it did indeed prevent the progression of cardiac disease.

“This tells us these amyloid beta-blocking drugs that have been developed for Alzheimer’s disease could be immediately repurposed for obesity-induced heart disease.

“Given these therapies already exist and have been safety tested in humans, it would be feasible to move directly to clinical trials.

“This will reduce the drug development process by around 10 years.”

Professor McGee is now seeking both grant funding and/or commercial support to advance this work.

Originally published as Alzheimer’s disease medication could treat obesity-induced heart disease, new study suggests