Alzheimer’s on trial A small number of Alzheimer’s interventions, some highlighted below,
are currently in Phase iii clinical trials, which are undertaken after preliminary studies show that
a drug is safe and may be effective. right now, more than 800 clinical trials — including those at
earlier stages of testing — are searching for potential Alzheimer’s therapies. Among those are
therapies that examine the effects of exercise, diet and inflammation-reducing drugs.
Potential Alzheimer’s therapies in Phase III clinical trials
Alpha-tocopherol
(Vitamin E)
Vitamin e may protect brain cells by scooping up toxic
free radicals.
Bapineuzumab
(AAB-001)
Multiple clinical trials are testing bapineuzumab, a
laboratory-designed antibody that binds to and removes
A-beta from the brain.
Harvested from blood donors, these naturally occurring
antibodies may reduce A-beta in the brain.
Found in red wine, this compound may protect brain cells
from damage. it is being tested along with glucose and
malate, which are thought to prime resveratrol for its
beneficial actions.
Solanezumab this drug is thought to bind to smaller, soluble assemblies of A-beta before they become plaques and remove
them from the brain.
Intravenous immunoglobulin
(IVIG, Gammagard)
Resveratrol
sourCe: www.CliniCAltriAls.goV/Ct2/HoMe
A-beta plaques in cognitively healthy
people raises doubts about A-beta as the
bad actor it was once assumed to be. So
does A-beta’s failure, in mice, to elicit the
kind of massive and widespread neuron
death seen in Alzheimer’s.
“We’ve filled mouse heads with
plaques, and oligomers for that matter,”
Herrup says. “And what we’ve created
is, at best, mild cognitive impairment….
If you go to the Alzheimer’s ward of any
institution, most of the residents there
would be ecstatic to be returned to the
level of function in our worst mouse
model.”
Another particularly troubling piece
of data is that, so far, lowering A-beta
levels in human brains hasn’t improved
brainpower. A drug called bapineu-
zumab, thought to shuttle A-beta out of
the brain, decreased amyloid plaques in
the brain but didn’t boost brainpower in
patients with mild to moderate disease, a
clinical trial published in Lancet Neurol-
ogy last year showed.
“The main issue is that none of
these amyloid-lowering therapies have
improved cognitive function,” Gandy
says. “If there had been a benefit to any
of the things that lowered amyloid, then
that would obviously put all the doubt
to rest.”
That’s not to say A-beta doesn’t have
a role in the disease. But in some cases
A-beta may not be leading the charge.
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