This is incredible.
BEC
CREW
1
SEP 2016
“A new drug trial for Alzheimer’s
patients has just been completed, and researchers are calling the results the
most promising yet in the fight against the disease. The drug targets amyloid deposits
- toxic proteins linked to the onset of Alzheimer’s - and after just 12 months,
patients on the highest dose had no detectable signs of these deposits.
“Not only that, but for the 20
early-stage Alzheimer’s patients who took the highest dose of the drug for more
than six months, there were indications that their cognitive decline and memory
loss had been slowed down.
“‘This is the best news we’ve had in my
25 years of doing Alzheimer’s research, and it brings hope to patients and
families affected by the disease,’ one of the researchers, neurologist Stephen
Salloway from Butler Hospital in Providence, Rhode Island, told
Nature. ‘Compared to other studies published in the past, the effect
size of this drug is unprecedented,’ another of the team, Roger Nitsch from
Zurich University, Switzerland, told
The Independent.
“Before we go into the details, let’s
be clear that this is just one trial with a small number of participants, and ‘cautiously
optimistic’ is the name of the game here. Nothing is confirmed until the
results are replicated in a much longer trial with a larger and more diverse
sample set, so while we can be excited about the incredible potential of this
drug, we need to wait for follow-up trials. So with that in mind, here’s what
happened.
“The team recruited 165 participants
who had been diagnosed with the early stages of Alzheimer’s disease to test the
efficacy of a drug based on an antibody
called aducanumab. Aducanumab has been shown to naturally occur in people who
age without experiencing significant cognitive decline, so the researchers
decided to see what would happen if they injected high doses of the antibody
into people with early-stage Alzheimer’s.
“It’s not clear how this antibody
works, but the team announced at
a recent conference that it appears to target amyloid deposits in the
brain, but not in the bloodstream. The hypothesis suggests antibodies that
attack amyloid in the bloodstream get sidetracked and never make it into the
brain,’ Karen
Weintraub explains over at Scientific
American. ‘By focusing on brain amyloid, aducanumab seems to be
able to cross into the brain to reach its target.’
“The 165 participants were split into
different groups, and some received the aducanumab drug in different doses, and
one group of 40 received a placebo. Of
the 103 patients who were given the drug once a month for up to 54 weeks,
they all experienced a reduction in the amount of amyloid deposits in their
brains. And the researchers found that the higher the dose, the more deposits
were cleared from the brain. In the group of 21 patients who received the
highest dose, no detectable signs of amyloid deposits remained in their brains
after a year.
“Similar results were reported in a
pre-trial mouse study, which saw mouse brains cleared of amyloid deposits after
aducanumab treatment. ‘This drug had a more profound effect in reversing
amyloid-plaque burden than we have seen to date,’ Alzheimer’s researcher Eric
Reiman from the Banner Alzheimer’s Institute in Phoenix, Arizona, who is not
involved in the study, told
Erika Check Hayden at Nature. ‘That is a very striking and encouraging
finding and a major advance.’
“No one’s entirely sure what
causes Alzheimer’s disease, but it’s thought to result from a buildup of
two types of lesions in the brain: amyloid deposits - or 'plaques' - and
neurofibrillary tangles. Amyloid deposits sit between the neurons as dense
clusters of beta-amyloid molecules - a sticky type of protein that easily
clumps together - and neurofibrillary tangles are caused by defective tau
proteins that clump up into a thick, insoluble mass inside the neurons. This
causes disruptions to the transportation of essential nutrients around the
brain, which is thought to bring on the cognitive decline and memory loss
associated with Alzheimer’s disease.
“Over the years, the roles of amyloid
deposits and neurofibrillary tangles in the onset of Alzheimer’s have been
debated, because it’s not yet clear if one causes the other, or if one has a
greater overall effect. But this new trial suggests that if you can get
rid of the amyloid deposits, you have a chance at stalling the progression of
the disease. The researchers report that they saw slower cognitive declines in 91
patients treated with the drug.
“‘Aducanumab also showed positive
effects on clinical symptoms,’ Nitsch
explained in a press statement. ‘While patients in the placebo group
exhibited significant cognitive decline, cognitive ability remained distinctly
more stable in patients receiving the antibody.’
“The results are definitely exciting,
but it’s time to replicate them in a larger group of patients. The team is now
recruiting another 2,700 patients from 20 different countries to participate in
a new 18-month trial, the results of which are expected in 2020.
“‘These results are the most detailed
and promising that we’ve seen for a drug that aims to modify the underlying
causes of Alzheimer’s disease,’ James Pickett, head of research at the
Alzheimer’s Society, who was not involved in the study, told
Ian Johnston at The Independent. ‘No existing treatments for
Alzheimer’s directly interfere with the disease process – and so a drug that
actually slows the progress of the disease by clearing amyloid would be a
significant step.’
“The results have been reported in Nature.”
The above article is from Science Alert.
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