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Cancer drug can 'REVERSE' Alzheimer's before it takes hold, study suggests: 'Could impact families, society, economy'
They key to stopping Alzheimer's disease before it begins could lie in a drug that doctors already use to treat another disease, a landmark new paper suggests.
Researchers from Penn State and Stanford used a type of cancer drug to repair one of the early systems that breaks down in dementia - how the brain uses energy.
The drugs, which worked to restore levels of sugar delivered to nerve cells, reinvigorated the brains of the mice treated with the therapy, protecting their memory and potentially reversing dementia.
This is the first treatment of its kind that promises to treat the causes behind Alzheimer's, not just managing the symptoms of the disease, the study authors said.
The researchers from Penn State (pictured) focused on an entirely new theory as to how Alzheimer's may begin - moving from treating symptoms of the disease to treating the cause
Early on in Alzheimer's disease, cells which deliver energy to neurons stop doing so as efficiently as they would in a normal brain. The researchers targeted this break down
This has potential implications for the nearly 7 million American's currently living with Alzheimer's disease.
By 2050, the Alzheimer's Association predicts that number will reach 13 million - and will cost Americans nearly $1trillion per year.
Dr Melanie McReynolds, a co-author of the paper and a Dorothy Foehr Huck and J. Lloyd Huck Early Career Chair in Biochemistry and Molecular Biology at Penn State, said: 'In the broader context of aging, neurological decline is one of the biggest co-factors of being unable to age healthier.'
The benefits of understanding and treating metabolic decline in neurological disorders will impact not just those who are diagnosed, but our families, our society, our entire economy.'
Right now, the drugs that exist to treat the disease focus on removing proteins in the brain, called beta-amyloid plaques.
But an increasing amount of neuroscientists suspect these plaques aren't causing dementia and are instead a symptom of the disease.
So treating these plaques is like giving Advil to someone with a cold. It might take away some of their discomfort, but it won't get the bug out of their system.
Instead, this treatment is trying to stop Alzheimer's before the symptoms - including memory loss, confusion and language loss- ever begin.
One of the many things that happen on a molecular level early on in Alzheimer's disease is that neurons stop getting as much sugar, or energy, as they need.
This makes them weaker and sicker, Dr Paras Minhas a resident at Memorial Sloan Kettering Cancer Center said.
The researchers looked to this energy-loss as a potential cause of Alzheimer's disease. In their paper, published in published in the journal Science, they targeted an enzyme called indoleamine-2,3-dioxygenase (IDO1), which they thought could be behind this break down.
They used a type of drug, called IDO1 inhibitors, which stop the enzyme from working as well and getting in the way of sugar being delivered to neurons.
This is the same kind of drug that is being developed to treat skin, breast and blood cancers. There aren't many of these drugs currently in use.
One, called Verzenio, which is used for breast cancer, runs about $15,000 per month without insurance. It's taken in pill form.
The researchers applied this kind of therapy to mice and to cells they grew in the lab that had signs of Alzheimer's. In both cases, the cancer drugs helped keep cells in the brain that feed neurons healthy - so that they could keep pumping out energy for neurons to use.
This stopped the telltale signs of disease, the beta-amyloid plaques, from forming, Praveena Prasad, a doctoral student at Penn State who contributed to the research, said.
The researchers tested this therapy in mice and in cells they had grown in the lab. Next steps will require testing the theory in more animals, and eventually, in humans
'We’re demonstrating that by targeting the brain’s metabolism, we can not only slow, but reverse the progression of this disease,' she said.
Part of the reason that dementia research is so difficult is because scientists have yet to determine what causes it.
The researchers don't claim that this loss of energy to brain cells is the sole cause behind Alzheimer's, but it is a new theory that could help them untangle the whole mystery.
And this lies in a drug we already have developed, Dr Katrin Andreasson, the lead author from the Stanford University School of Medicine, said.
Dr Andreasson said: 'Inhibiting this enzyme, particularly with compounds that have been previously investigated in human clinical trials for cancer, could be a big step forward in finding ways to protect our brains from the damage caused by aging and neurodegeneration.'
Still, they'll need to test it in more complex animal models, and eventually in humans before it proves widely useful. The drugs could still fail at any point in that process
And even if it succeeds the next rounds of testing, it will still be years before this becomes a widely available treatment for dementia.
Some studies have said that it takes on average 7.5 years for a drug to get through clinical trials in the US. Though because some kinds of IPO1 drugs have already been deemed safe in humans, it likely won't be that long.