May 10, 2007
Alzheimers Disease Caused By Nerve Demyelination?

A UCLA prof thinks decay of a nerve insulating material called myelin might be a key step that leads to Alzheimer's Disease.

Wisdom comes with age (doesn't it?), but not without a process that takes place in the brain called myelination. Myelin is the fatty sheath that coats the axons of the nerves, allowing for efficient conduction of nerve impulses. It is key to the fast processing speeds that underlie our higher cognitive functioning, including, yes, wisdom.

Myelination continues sheathing axons until we reach the age of about 50, but in these later stages, the myelin becomes more and more susceptible to damage. Now, in a report in the April issue of the journal Alzheimer's & Dementia, Dr. George Bartzokis, UCLA professor of neurology, suggests that it is the breakdown of this late-stage myelin that promotes the buildup of toxic amyloid-beta fibrils that eventually deposit in the brain and become the plaques which have long been associated with Alzheimer's disease.

These amyloid products in turn destroy more and more myelin, according to Bartzokis, disrupting brain signaling and leading to cell death and the classic clinical signs of Alzheimer's. If correct, the research suggests a broader approach to therapeutic interventions for the disease.

If myelin breakdown is behind Alzheimer's then that strongly suggests to me that brain rejuvenation therapies that repair and replace myelin would be most effective at preventing and stopping Alzheimer's.

Late stage added myelin is thinner and breaks down more easily.

"Myelination of the brain follows an inverted U-shaped trajectory, growing strongly until middle age. Then it begins to breakdown," Bartzokis said. "Before the advent of modern medicine, very few persons lived beyond age 50 and therefore, as a species, we evolved to continue myelinating over our entire natural life span."

As a result, the volume of myelinated white matter increases to a peak at about age 50, then slowly begins to reverse and decline in volume as we continue to age. The myelin that is deposited in adulthood ensheaths increasing numbers of axons with smaller axon diameters, and so spreads itself thinner and thinner, he said. As a result, it becomes more susceptible to the ravages of age in the form of environmental and genetic insults and slowly begins to break down.

Your myelin slowly breaks down after age 50. That, by itself, is thoroughly disgusting even before we consider the threat from Alzheimer's. The brain is our most powerful tool. Our brains become less powerful. In the process of its decay and aging we become less capable and lose parts of who we are. Shouldn't we try much harder with research funding to find ways to stop and reverse brain aging?

Dr. Bartzokis found that the areas of the brain with the latest myelin formation are the areas where amyloid plaques form.

Oligodendrocytes and myelin have the highest levels of iron of any brain cells, Bartzokis said, and circumstantial evidence supports the possibility that brain iron levels might be a risk factor for age-related neurodegenerative diseases like Alzheimer's. In the study, he suggests that myelin breakdown in the late-myelinating regions releases iron, which promotes the development of the toxic amyloid oligomers and plaques, which in turn destroy more myelin.

Bartzokis tested his hypothesis by examining published images of amyloid deposition acquired in living individuals; the images were made using radiolabeled ligands molecules that bind to amyloid plaques in the brains of Alzheimer's patients. Next, he compared the physical location of these plaques to much earlier work published in a the Lancet in 1901 that mapped the locations in the brain where late-stage myelination occurs. The two matched up perfectly.

Stem cells and gene therapy are both strong contenders to some day serve treatments to re-myelinate aging brains. We need faster rates of research into both approaches.

Treatments that stop and reverse nerve demyelination will some day boost worker productivity and increase the rate of economic growth. We should try 10 times harder to develop those treatments.

Share |      Randall Parker, 2007 May 10 10:58 PM  Brain Alzheimers Disease


Comments
Nick said at May 11, 2007 4:37 PM:

I've read previously that there are links between MS and Alzheimer's. This is consistent with that.

I wonder if things that help MS, like Vitamin D and curcumin, would help Alzheimer's. Isn't there a correlation between latitude and Alzheimer's?

Bob Badour said at May 12, 2007 5:55 AM:

Prophylactic B12 injections of aging adults seem even more important as time goes on. B12 deficiency can lead to myelopathy, and the progression of my grandfather's dementia followed that path exactly: myelopathy->demyelination->dementia.

For every older adult: If your doctor doesn't stick you with a B12 injection on every visit, ask your doctor to. It's cheap. It's safe. It's almost certainly beneficial.

rsilvetz said at May 12, 2007 10:16 AM:

Bob,

That's one hell of a comment and i think you're right -- I've found in Pubmed mixed data. Homocysteine is emerging as an independent risk factor. Probably the inflammatory effects on the microvasculature. Higher B12/B6 is has a loose association with the dementia angle. Increasing levels have lower incidence.

However, nobody seems to have followed a supplementation angle over the long term, so we don't have the evidence on the physiological/supra-physiological angle.

Which is a pity because I think your thought has real value.

Randall Parker said at May 12, 2007 2:08 PM:

Guys,

I had one older family member who had measured low B12 (even though he ate too much meat) and the doctor gave him a shot. But then it did not become routine to get the shot. I'd ask to have him mention it to his doctors. It seemed like such a basic thing to do routinely. But I can save based on experience with several doctors that they did not do so in this case.

The B12 absorption problem seems fairly widespread with age. Vitamin D deficiency is more widespread because it hits all ages. But B12 is probably in the top 5 list of nutrient deficiencies in America today.

Audacious Epigone said at May 12, 2007 6:26 PM:

Dr. Bartzokis found that the areas of the brain with the latest myelin formation are the areas where amyloid plaques form.

Which seems to make perfect sense in light of how in people suffering from Alzheimer's, the most recent memories are the first to go.

Doug said at May 14, 2007 11:34 AM:

The problem of nonabsorption of vitamin B-12 may already be completely resolved and the periodic injections of large doses may now be avoidable. As a means of elevating and sustaining serum vitamin B-12, look into oral methylcobalamin; I think the Life Extension Foundation's buyers' club is just one of many sources. According to LEF's information, the tissues of the mouth absorb methylcobalamin; I think LEF says further that allowing a tablet containing this form of vitamin B-12 to dissolve in one's mouth, rather than swallowing it, allows the vitamin B-12 to spread widely throughout the body without first encountering the liver, which otherwise would convert much of it to its metabolites, in what's sometimes called "the first-pass effect."

I do take methylcobalamin, but since I don't know my before-and-after levels of serum vitamin B-12, my own case isn't useful in support or refutation of methylcobalamin's greater absorbability. However, I have a near relative who was formerly deficient in vitamin B-12 because of a digestive problem; she formerly supplemented B-12 by injection, but began taking B-12 orally as methylcobalamin. She told me recently that her physician had re-tested her serum B-12 level; if she understood her results and I understood her correctly, the test showed that her serum level is now toward the high end of the healthy range.

So, then, anyone who's worried about vitamin B-12 deficiency may consider reading about methylcobalamin and discussing it with one's physician. It seems effectively supplementing vitamin B-12 orally on some frequent basis would eliminate the need for either a patient or a physician to remember the need for an injection and take the initiative to arrange it.

Fred said at May 14, 2007 4:26 PM:

Re: oral B-12. So-called "sublingual" tablets are what you want.

Leslie Feldman said at May 20, 2007 12:38 AM:

Here it is again but Dr. Bartzokis and I have communicated about his ideas and his research. The way to prevent Alzheimer's disease is for men to father all their babies by their early 30s. http://ageofthefatherandhealthoffuture.blogspot.com/search?q=Alzheimer%27s


The issue is that the older man will have sperm that has undergone more divisions and therefore had more chances to have mutations.
The COMPLEXITY of the myelination process makes it more vulnerable to mutations. I am not talking of one specific mutation. Many things could MANIFEST in the myelination or myelin breakdown process because it is so vulnerable - something going slightly wrong will impact it while it will not impact bone growth or the heart. A good example is ApoE4 - whatever else it may affect, it manifests in the reduced capacity of myelin repair and earlier onset of AD.

Hope this clarifies things.
.

George B


Fund Alzheimers said at May 13, 2008 1:38 AM:

I think USA should fund embryonic stem cell research, that would be a big change in the fate of lethal diseases like cancer, alzheimer's or parkinson's in the whole world. Gene therapy is also a possible way, but it is harder to find solutions on the gene level which is mostly beyond our knowledge. Thus stem cells are the future of the research, and US government should put ethics issues aside and give importance to people's lives

milesrf said at April 28, 2009 6:26 PM:

A project that lets the public use their computers to help with Alzheimer's research:

http://boinc.bakerlab.org/rosetta/

Rather memory-hungry though; not recommended for computers with less than 1 GB of memory

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