
A New Tack to Stave Off Alzheimer's Years Before the First Symptom - mrestko
https://blogs.scientificamerican.com/talking-back/a-new-tack-to-stave-off-alzheimer-s-years-before-the-first-symptom/
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helloworld
_[W]e know there is little relationship between the amount of amyloid in one’s
brain and your memory function. In fact, those “super-agers”—your 95-year-old
great-great-aunt who finishes the crossword puzzle in 20 minutes, is president
of the bridge club and has a better golf handicap than you—may have just as
many amyloid plaques in her brain as AD patients._

Another AD researcher, Rudolph Tanzi, recently made the same point, suggesting
that it's the inflammation caused by these plaques in some patients that leads
to dementia:

[http://www.aarp.org/health/brain-
health/info-2016/alzheimers...](http://www.aarp.org/health/brain-
health/info-2016/alzheimers-cure-research-drugs-hd.html)

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stretchwithme
The right diet can reduce the risk of Alzheimer’s by 54%.

[http://www.webmd.com/alzheimers/features/mind-diet-
alzheimer...](http://www.webmd.com/alzheimers/features/mind-diet-alzheimers-
disease)

~~~
pcunite
You eat things from these 10 food groups:

• Green leafy vegetables

• Other vegetables

• Nuts

• Berries

• Beans

• Whole grains

• Fish

• Poultry

• Olive oil

You avoid:

• Red meat

• Butter and margarine

• Cheese

• Pastries and sweets

• Fried or fast food

~~~
dcosson
The study shows that this diet may be sufficient for a better outcome for
altheimers, but I'm skeptical that this in its entirety is necessary. Research
on metabolic diseases is more and more pointing towards fats not being much of
a factor, and sugar and too many total calories (from any sources) being large
factors.

And ketogenic diets have shown some effect at fighting altheimers, other
metabolic diseases, and even some cancers, which is why treating fat as the
enemy doesn't make a whole lot of sense to me.

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reasonattlm
This is sort of illustrative of a prevalent failure mode in high level R&D
strategy in medicine.

What they are doing is reasonable as an immediate extension of trying to map
the disease process front to back, which is what pure research should be
doing. The outcome of that, however, tends to be that people end up
manipulating biochemistry to slow the disease process rather than fix it. You
can get useful results out of this - see statins, for example. But you can't
get cures. People who take statins will still end up in the same bad place in
the end, just a little later. Also, it is very expensive to find safe new
states for cellular operation that provide a decent benefit:harm ratio.

One right thing to do in Alzheimer's is map the whole thing end to end, them
make a decision on what to do. An enormous task that is basically the same
thing as understanding the human brain end to end - which is a good thing in
and of itself, and if Alzheimer's provokes that work (in the same way that
AIDS provoked analogous major efforts to understand viral biochemistry) then
good. But in the short term that doesn't produce useful therapies.

The other right thing to do is to identify the fundamental differences between
young, non-diseased tissue and aged, diseased tissue and work to revert them -
even if you don't know how they are causing harm. Successful removal will tell
you a great deal about the significance, and steer other research, and in the
best case produce a useful therapy. Thus a focus on amyloid and tau, and
immunotherapies to clear them, and dysfunctions in cerebrospinal fluid
clearance mechanisms, with approaches ranging from simple mechanical
adjustment of fluid drainage channels behind the nose to proposed stem cell
therapies for the choroid plexus to addressing immunosenescence in the brain's
immune system.

However, Alzheimer's is such a multifaceted condition that researchers tend to
focus on reverting one of these items, then don't produce wondrous benefits
because the other mechanisms are still in play, and then the people who prefer
to slow disease progression instead arrive to argue that this means they
shouldn't look at this direct approach of reverting differences. To fix
Alzheimer's will likely require clearance of both amyloid and tau, and even
then it is likely that since 60% of sufferers also have vascular dementia, it
will be challenging to produce good trial outcomes under the present
regulatory system.

If damage repair doesn't work, that means you're not repairing enough of the
damage.

~~~
ktRolster
_One right thing to do in Alzheimer 's is map the whole thing end to end, them
make a decision on what to do._

I think you're underestimating the difficulty of that task. Not only is
current technology inadequate for mapping the brain, even if we did draw the
lines, we would still be far from understanding it. Even _C. Elegans_ took
over a decade to map, and while it's true that our technology is better, it is
still not up to the task of mapping the brain.

If we waited until the brain were mapped to make any progress would mean
delaying much progress.

~~~
reasonattlm
That's kind of the point. That is exactly what's happening in the research
community, plus the inefficiency of people stepping off the mapping process as
soon as they find some mechanism that might slightly slow disease progression,
and then focusing on that rather than something that might clean up the damage
instead of slowing it down.

Not enough of the research community is doing the other thing, the repair and
reversion of differences between old and young tissues carried out in advance
of full understanding, so as to aim at cures rather than delay.

Alzheimer's, funnily, is in a much better position than most other age-related
diseases because a large chunk of the mainstream of the research effort is
actually directed towards a repair-of-the-differences approach - removal of
amyloid via immunotherapy in this case. That choice of strategy isn't true for
heart disease, diabetes, dementia, etc, etc. If we want to see cures for age-
related disease, there must be a sweeping change in the research community's
high level strategy, towards repair of fundamental damage that distinguishes
old tissues from young tissues, and away from tinkering with the disease state
to slow it down or to compensate for some of its effects.

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untilHellbanned
Ahh ye old biologist doing ye old refuctionist science.

Good luck on ye old calcium drug preventing more Alzheimer's then it does
causing ye old bad something else.

I always find it interesting to figure out why work like this gets attention
compared to the 87,000 other approaches for important disease X. This work
seems particularly preliminary.

Silly humans distracting each other. It's like we are the Washington Generals
and Disease is the Harlem Globetrotters.

