The findings, published in Nature Communications, upend prior beliefs that amyloid beta only damages brains and open new treatment possibilities for a previously untreatable condition.
“As part of this world-first study, laboratory tests have revealed that amyloid beta is secreted from fat tissue into the bloodstream,” said lead author Professor Sean McGee, Deakin School of Medicine. “We looked at both lean mice and mice that were fed a high fat diet that results in obesity, and it was clear that obese mice had much higher levels of amyloid beta in their blood.”
Further tests proved the protein itself induces heart disease by accumulating in energy-producing mitochondria and preventing cells from generating enough energy to pump blood.
“To our knowledge, this is the first time that amyloid beta has been implicated in a disease that is not Alzheimer’s,” Professor McGee stated. “It was thought amyloid beta’s negative effects were restricted to the brain.”
Because amyloid beta has been heavily targeted for Alzheimer’s therapies, Professor McGee believes rapid repurposing for obesity heart disease is achievable.
“As amyloid beta is linked to Alzheimer’s Disease there are numerous therapies and drugs developed in recent years,” he explained. “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.”
This means Alzheimer’s drugs could skip 10 years of development by proceeding straight to human trials for obesity heart patients. Professor McGee is now seeking funding and pharma partners to progress his work.
Obesity-induced heart disease has to now been considered an untreatable condition however this study shines a light on how it develops and provides a viable pathway for its treatment,” he said. “We are working to provide new hope to patients with this very challenging condition.”