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New model for brain aging?

brain myelin mind aging brain

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#1 Lazarus Long

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Posted 29 March 2019 - 02:37 PM

When understanding the aging process we need to look at multiple, both related and independent mechanisms that are at work. One of the most impactful aspects of the aging process is how the loss of mental capacity relates to the quality and the quantity of life. This article addresses evidence for an alternative understanding of what is happening to the brain as it ages but doesn't really address the causal aspects.

This is an instance where there might be a confusion of correlation and causality.



Summary: New patterns of brain ageing across the human lifespan have been revealed by researchers analysing microstructural changes in the brain’s white matter.

Source: Goldsmiths, University of London

Dr Marinella Cappelletti from Goldsmiths, University of London, University of Oxford’s Dr Vyacheslav Karolis, and colleagues, mapped and analysed myelin content in the brains of almost 100 healthy adults aged 20 to 74.

A report on their research is published in the journal Neurobiology of Ageing.

Myelin is a substance that wraps around nerve fibres, increasing the speed of electrical communication between neurons. Its light colour gives a name to the brain tissue known as white matter – a collection of fibres which connects distant brain areas. Myelin loss, through normal ageing or through disease, typically causes neurological dysfunction.

Using magnetisation transfer concentration (a brain imaging marker sensitive to myelin content), the research team mapped myelin content across the brain in people of different ages and demonstrated that healthy ageing is not a steady, or uniform, process.

Dr Karolis et al have also identified a new pattern of brain ageing which shows that regions of the brain’s white matter that are more lateral (toward the side) start declining from about the mid-40s, although the decline is relatively slow.

In contrast, white matter in the ventral, or deeper, areas of the brain showed relatively stable myelin levels until around the late-50s, at which point age-related changes appear, and decline continues quite rapidly. The researchers have termed this pattern the lateral-to-ventral gradient of ageing.

They also found a moderate ageing effect in the temporal lobe, an area of the brain often associated with neurodegeneration (the loss of structure or function in neurons); this suggests that brain regions which show myelin loss in healthy ageing are different from those showing pathological changes.

Dr Cappelletti said: “The study provides a closer link between developmental and ageing processes. The ventral-to-lateral sequence has previously been observed in the process of myelin development with myelination progressing from deep to lateral areas. Here we show a clear reversal of this pattern in ageing, and provide benchmark data which may help to distinguish between healthy and pathological ageing, and also highlight the importance of looking at ageing from mid-life.”
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#2 Phoebus

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Posted 29 March 2019 - 05:51 PM

So aging here is basically demyelination of the brain, which is the same thing that happens with MS 


They recently discovered what block remyelination of brain tissues, I wonder if this is the same thing happening in all aging poeple? 



A molecule responsible for preventing the repair of white matter in the brain, a process critical to treating multiple sclerosis (MS) and cerebral palsy, has been identified.

The research, “A TLR/AKT/FoxO3 immune-tolerance like pathway disrupts the repair capacity of oligodendrocyte progenitors,” was published in The Journal of Clinical Investigation.


White matter in the brain’s white matter is composed of nerve fibers. Its color comes from myelin, the protective layer wrapping nerve fibers that works to ensure proper cell communication. Damaged myelin is a hallmark of MS and other disorders.


Myelin is produced by cells called oligodendrocytes. Research shows that, in cases of chronic white matter injury, oligodendrocyte progenitor cells (OPCs) — the precursor cells of oligodendrocytes — accumulate in lesion areas but are unable to produce myelin. Scientists believe this is due to the presence of fragments from a very large molecule called hyaluronic acid (HA); these small fragments also accumulate at lesion sites.

Now, researchers studied how these HA fragments block myelin repair.

Results showed that one specific-size fragment of HA affected OPCs. Treating rat cells modeling white matter disease with this specific fragment initially activated myelin formation, then completely shut down.


Researchers noted that this is similar to the immune tolerance mechanism, which is used by the immune system to prevent severe tissue injury from an ongoing, damaging immune response.

“We showed that HA creates not just a roadblock to myelin repair after injury, it also shuts down all of the possible detours,” Stephen Back, the study’s senior author and a professor of pediatrics and neurology at the Oregon Health & Science University in Portland, said in a press release. “Tolerance can be helpful in preventing the brain from repairing itself too quickly, but in some disease conditions, it can turn into a detrimental response.”

“Strategies to reverse this tolerance-like state appear to represent a novel approach to promote myelin regeneration,” the researchers wrote.


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#3 Phoebus

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Posted 29 March 2019 - 05:58 PM

Now here is a study from 2012 which shows that out of control hyaluronidase that cause the hyaluronic acid to be broken down that is the issue. 


So inhibiting hyaluronidase (which would hopefully allow HA to do its part in repairing myelin) may be a potential treatment for brain aging. 



Sherman's lab has been studying MS and other conditions where myelin is damaged for more than 14 years. In 2005, he and his research team discovered that a sugar molecule, called hyaluronic acid, accumulates in areas of damage in the brains of humans and animals with demyelinating brain and spinal cord lesions. Their findings at the time, published in Nature Medicine, suggested that hyaluronic acid itself prevented remyelination by preventing cells that form myelin from differentiating in areas of brain damage.

The new study shows that the hyaluronic acid itself does not prevent the differentiation of myelin-forming cells. Rather, breakdown products generated by a specific enzyme that chews up hyaluronic acid -- called a hyaluronidase -- contribute to the remyelination failure.

This enzyme is highly elevated in MS patient brain lesions and in the nervous systems of animals with an MS-like disease. The research team, which included OHSU pediatric neurologist Stephen Back, M.D., and OHSU neuroscientist Steve Matsumoto, Ph.D., found that by blocking hyaluronidase activity, they could promote myelin-forming cell differentiation and remyelination in the mice with the MS-like disease. Most significantly, the drug that blocked hyaluronidase activity led to improved nerve cell function.


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