Major Breakthrough: Alzheimer's, Parkinson's Stopped With New DrugThursday, 10 Oct 2013 01:16 PM In a development that's being hailed as a major breakthrough in the search for an Alzheimer's disease cure, British researchers say they have identified a drug-like compound that combats the debilitating condition and may also work against other neurodegenerative illnesses like Parkinson's.
In a new study, published today in the journal "Science
Translational Medicine," scientists from the Medical Research
Council Toxicology Unit at the University of Leicester have found
the compound can effectively "switch off" the defective neurological
processes in the brains of dementia patients that lead to the death
of brain cells.
The discovery could pave the way for new treatments for the
condition that strikes millions of Americans and tens of millions
more around the world.
"We’re still a long way from a usable drug for humans — this
compound had serious side effects," noted lead researcher Giovanna
Mallucci, in a university press statement. "But the fact that we
have established that this pathway can be manipulated to protect
against brain cell loss first with genetic tools and now with a
compound, means that developing drug treatments targeting this
pathway for … neurodegenerative diseases is now a real possibility."
Prior research by the MRC team had found the buildup of certain
misshapen proteins in the brains of mice can trigger the kind of
brain cell death seen in Alzheimer's patients. By blocking the
production of those proteins, they found they could effectively
protect the brain cells of the mice and allow them to live longer.
For the new study, the researchers gave an oral drug-like compound
to mice with dementia-like symptoms, hoping to block the defective
brain-signalling processes in the same way. The compound, which had
originally been developed by GlaxoSmithKline for a different
purpose, was able to enter the brain from the bloodstream and halt
the disease, throughout the whole brain. It also produced weight
loss in the mice and mild diabetes, due to damage to the pancreas,
the researchers said.
Although the compound was tested in mice, researchers said the same
principles apply to the brains in people with debilitating brain
diseases such as Alzheimer's or Parkinson's.
"Our previous study predicted that this pathway could be a target
for treatment to protect brain cells in neurodegenerative disease,"
said Mallucci. "So we administered a compound that blocks it to mice
with [dementia]. We were extremely excited when we saw the treatment
stop the disease in its tracks and protect brain cells, restoring
some normal behaviors and preventing memory loss in the mice."
Hugh Perry, chair of the MRC’s Neuroscience and Mental Health Board,
said he is confident future research will determine ways to blunt
the negative side effects of the compound and that the findings have
broad implications that go beyond treating Alzheimer's patients.
"Misshapen proteins in prion diseases and other human
neurodegenerative disorders, such as Alzheimer's and Parkinson's,
also over-activate this fundamental pathway controlling protein
synthesis in the brains of patients," he said. "Despite the toxicity
of the compound used, this study indicates that, in mice at least,
we now have proof-of-principle of a therapeutic pathway that can be
targeted.
"This might eventually aid the development of drugs to treat people
suffering from dementias and other devastating neurodegenerative
diseases."
According to the American Institute on Aging, as many as 5.1 million
people in the U.S. have Alzheimer's disease. There is no current
cure and studies of drugs to treat the condition have been
disappointing in recent years. Existing treatments may slow the
advance of the disease or modify the symptoms.
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