(wow) Words Of Wonders Level 2982 Answers – Here at SoPD, we regularly talk about the ‘bad boy’ of Parkinson’s – a protein called alpha-synuclein.
Twenty years ago this year, genetic changes in the alpha-synuclein gene were identified that increase the risk of Parkinson’s disease. Additionally, the protein alpha-synuclein has been found to be present in Lewy bodies found in the brains of people with Parkinson’s disease. Later, alpha-synuclein was regarded as the villain in this neurodegenerative condition and received much attention from the Parkinson’s research community.
(wow) Words Of Wonders Level 2982 Answers
He met this statement with a smile rather than a shock. And I was waiting for the last one, as a transition from
Etcmagazine_volume20_issue10 By Sara Sullivan
When asked to explain myself, I told him that I wanted to explore awareness, as Lao Tzu (the supposed author of
This answer also made him laugh (no doubt he thought Simon had done a bit of homework to sound like he knew what he was talking about).
Most religions teach philosophies and doctrines that actually define a person. Taoism – which dates back to the 4th century BC – turns this idea on its head. It begins by teaching one concept: the Tao (or “path”) is undefined. And then follows the suggestion that each person must discover that on their own terms. Given that most people would prefer a more specific definition in their lives, I understand that many people will not take this approach.
Personally, I really like the idea that the Tao is the only principle and everything else is its righteous expression.
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Oh, and don’t worry, I won’t bore you with any more philosophical nonsense – Taoism is an idea I’m exploring as part of a horribly clichéd mid-life crisis I’m going through (my original wife’s response was all “why don’t you just be normal Why don’t you buy a motorcycle or something?”).
However, I’m sharing it because this introduction provides an easy segway to what we’re actually going to talk about in this post.
You see, some Parkinson’s researchers believe that relief from neurodegenerative conditions like Parkinson’s can come from only one source:
This is a fluorescent image of two cells stained with two different colors: one shows
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The cell is the command center of the cell where the DNA is stored. But microtubules may be new to many readers.
Microtubules are highways and bypasses inside cells. They are structures inside cells that are involved in cellular and intercellular transport. That is, these skeletal structures help move cells from one place in the body (“cellular transport”), but they also help move proteins from one place inside the cell (“intracellular transport”). Also, microtubules play an important role in cell division.
TAU is a protein that is abundant in the brain. It is formed from the RNA (instructions for making proteins) of the MAPT gene located on chromosome 17.
TAU protein is a microtubule-associated protein that functions by stabilizing major and minor pathways in cells. Basically, these proteins assemble the pathways that allow vesicles (the little sacs I mentioned above) to move around the cell (with the help of transporter proteins like kinesin).
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In both cases, there is an accumulation of the protein TAU, which accumulates and forms clusters (or “aggregates”) similar to our old friend, the protein alpha-synuclein associated with Parkinson’s disease (click here for a good review article on this topic).
In this study, researchers analyzed post-mortem brains of two people with Huntington’s disease who had undergone stem cell transplants 9 and 12 years before death. They also examined brain sections from two people with Parkinson’s disease who had cell transplants 18 months and 16 years before they died (of natural causes). I previously discussed how alpha-synuclein aggregates were found in dopamine neurons in cell transplants from people with Parkinson’s disease (click here to read that post), but no one had looked at TAU in this context before this report.
Interestingly, when the researchers looked at the localization of TAU protein in Huntington’s disease brains, they found TAU aggregated inside transplanted cells. That is, somehow the healthy transplanted cells took on one of the pathological features of Huntington’s brain. Similarly, researchers also found aggregates of TAU protein in brain transplants of a 16-year-old Parkinson’s disease patient. Interestingly, they found none in 18-month-old transplants, suggesting that TAU clustering may be a very slow process.
Therefore, the idea that alpha-synuclein moves from cell to cell as Parkinson’s disease progresses may also apply to other proteins such as TAU.
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And TAU aggregation is certainly not unique to Alzheimer’s or Parkinson’s disease. And now many studies show that TAU may be involved in other neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS; a motor neuron disease; click here to read more about it) and multiple sclerosis (click here to read more about it).
It is still under investigation. And there is evidence that TAU protein levels naturally increase in the aging brain (source).
PMID: 20599975 (This article is open if you want to read it)
In this study, the researchers wanted to investigate where TAU aggregates are found in the postmortem brain. They compared the brains of people with Parkinson’s disease and those who died of Parkinson’s disease with dementia (PDD) to the brains of healthy controls. They found that brain levels of alpha-synuclein were higher in both Parkinson’s disease and PDD, particularly in PDD, which had consistently higher levels than in Parkinson’s brain in all brain regions analyzed.
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Interestingly, however, higher levels of TAU aggregation were found only in the striatum of Parkinson’s patients and PDD brains when brains were compared to healthy controls.
The researchers were unable to detect any higher levels of TAU aggregates in other brain regions in Parkinson’s disease brains or PDD brains, despite seeing higher levels of alpha-synuclein. And this result is very different from brains with Alzheimer’s disease, where higher levels of TAU aggregates are seen more globally – in different brain regions. The researchers concluded that their “data show a limited expression of tauopathy in PD and PDD brains, possibly restricted to dopaminergic neurons in the nigrostriatal region” (the nigrostriatal region is the substantia nigra where dopamine neurons are located and the striatum where dopaminergic neurons. The neurons release most of their dopamine).
And a recent research report indicated similar differences between Alzheimer’s, Parkinson’s and PDD (click here to read this report).
There appears to be some “co-localization” (both in the same place) of alpha-synuclein and TAU protein in the brain of Parkinson’s patients:
The Tau Of Parkinson’s
In this study, researchers analyzed postmortem brains of people who died of Parkinson’s disease. The researchers compared where alpha-synuclein and TAU are found. They found that regardless of the stage of Parkinson’s disease (newly diagnosed or chronic disease), TAU staining was present in Lewy bodies – the dense, spherical clusters of proteins characteristic of the Parkinson’s disease brain – in 80% of cases. And in most cases, TAU was located in the periphery of Lewy bodies, not in the nucleus (similar to alpha-synuclein).
Interestingly, the researchers found that the proportion of Lewy bodies with TAU protein was highest in neurons most vulnerable to Parkinson’s disease (such as the nucleus accumbens and nucleus basalis of Meynert, the two brain regions most affected by Parkinson’s disease), and the most. A lower number of neurons shows resistance to Parkinson’s disease.
Despite this research, some studies have shown that TAU and alpha-synuclein interact to form a dangerous pair in terms of neurodegeneration:
PMID: 24430504 (This article is open if you want to read it)
Oakley Press 04.19.19 By Brentwood Press & Publishing
In this study, the researchers used genetically engineered flies to look at the effects of a combination of TAU and alpha-synuclein. They found that high levels of human alpha-synuclein production had no effect when looking at the flies’ eyes (compared to untreated control flies). But when researchers gave flies high doses of the human protein TAU, it shrank the eyes.
However, an interesting result was obtained when the researchers produced flies that produced high levels of both proteins. The eyes were smaller and the surface of the eyes was rougher than when TAU flew alone (see image below).
The researchers assessed the flies’ motor performance (their ability to fly) and again found that instilling high levels of human alpha-synuclein in the flies did not affect flight ability (compared to non-engineered control flies).
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