New molecule could save brain cells from neurodegeneration, stroke (cancer, versus, nerve)

[Brian.Pearson]

...One microRNA jumped out at them, an entity called miR-29, which at that time had never before been implicated in preventing apoptosis. When the researchers injected their new molecule into young neurons, which are able to die if instructed, they found that the cells became resistant to apoptosis, even in the face of multiple death signals...

[baystater]

This molecule, a tiny strand of nucleotides called microRNA-29 or miR-29, has already been shown to be in short supply in certain neurodegenerative illnesses such as Alzheimer’s disease and Huntington’s disease. Thus, the discovery could herald a new treatment to prompt brain cells to survive in the wake of neurodegeneration or acute injury like stroke.

Deshmukh is currently developing mouse models where miR-29 is either “knocked-out” or overactive and plans to cross them with models of Alzheimer’s disease, Parkinson’s disease and ALS to see if it can prevent neurodegeneration.

It's early yet.....but lets see where the research goes.

I've see most of these diseases near their ending stages with the exception of ALS (seen fresh stokes as well.) And let me tell you. These diseases/injuries are absolutely horrible. To me it just completely robs people of their lives. I hope that this mircoRNA-29 has some factor in helping prevent death/injury to the brain.

"If we don't play God, who will?"
James Watson Co-founder of the structure of DNA.

[d-boy-80]

Originally Posted by Brian.Pearson

...One microRNA jumped out at them, an entity called miR-29, which at that time had never before been implicated in preventing apoptosis. When the researchers injected their new molecule into young neurons, which are able to die if instructed, they found that the cells became resistant to apoptosis, even in the face of multiple death signals...

The link is not working for me

[baystater]

Originally Posted by d-boy-80

The link is not working for me

Here's the text.

New molecule could save brain cells from neurodegeneration, stroke
This discovery could herald a new treatment to prompt brain cells to survive in the wake of neurodegeneration or acute injury like stroke.


click to enlarge
A fluorescently labeled neuron in which the apoptosis pathway is inhibited. Image source: Deshmukh lab, UNC. Media contacts: Les Lang, (919) 966-9366, llang@med.unc.edu; Tom Hughes, (919) 966-6047, tahughes@unch.unc.edu

Tuesday, Jan. 18, 2011

CHAPEL HILL, N.C. – Researchers at the University of North Carolina at Chapel Hill have discovered a molecule that can make brain cells resistant to programmed cell death or apoptosis.

This molecule, a tiny strand of nucleotides called microRNA-29 or miR-29, has already been shown to be in short supply in certain neurodegenerative illnesses such as Alzheimer’s disease and Huntington’s disease. Thus, the discovery could herald a new treatment to prompt brain cells to survive in the wake of neurodegeneration or acute injury like stroke.

“There is the real possibility that this molecule could be used to block the cascade of events known as apoptosis that eventually causes brain cells to break down and die,” said senior study author Mohanish Deshmukh, PhD, associate professor of cell and developmental biology.

The study, published online Jan. 18, 2011, in the journal Genes & Development, is the first to find a mammalian microRNA capable of stopping neuronal apoptosis.

Remarkably, a large number of the neurons we are born with end up dying during the normal development of our bodies. Our nerve cells must span great distances to ultimately innervate our limbs, muscles and vital organs. Because not all nerve cells manage to reach their target tissues, the body overcompensates by sending out twice as many neurons as required. The first ones to reach their target get the prize, a cocktail of factors needed for them to survive, while the ones left behind die off. Once that brutal developmental phase is over, the remaining neurons become impervious to apoptosis and live long term.

But exactly what happens to suddenly keep these cells from dying has been a mystery. Deshmukh thought the key might lie in microRNAs, tiny but powerful molecules that silence the activity of as many as two-thirds of all human genes. Though microRNAs have been a hotbed of research in recent years, there have been relatively few studies showing that they play a role in apoptosis. So Deshmukh and his colleagues decided to look at all of the known microRNAs and see if there were any differences in young mouse neurons versus mature mouse neurons.

One microRNA jumped out at them, an entity called miR-29, which at that time had never before been implicated in preventing apoptosis. When the researchers injected their new molecule into young neurons, which are able to die if instructed, they found that the cells became resistant to apoptosis, even in the face of multiple death signals.

They then decided to pinpoint where exactly this molecule played a role in the series of biochemical events leading to cell death. The researchers looked at a number of steps in apoptosis and found that miR-29 acts at a key point in the initiation of apoptosis by interacting with a group of genes called the BH3-only family. Interestingly, the microRNA appears to interact with not just one but as many as five members of that family, circumventing a redundancy that existed to allow cell death to continue even if one of them had been blocked.

“People in the field have been perplexed that when they have knocked-out any one of these members it hasn’t had a remarkable effect on apoptosis because there are others that can step in and do the job,” said Deshmukh. “The fact that this microRNA can target multiple members of this family is very interesting because it shows how a single molecule can basically in one stroke keep apoptosis from happening. Interestingly, it only targets the members that are important for neuronal apoptosis, so it may be a way of specifically preserving cells in the brain without allowing them to grow out of control (and cause cancer) elsewhere in the body.”

Deshmukh is currently developing mouse models where miR-29 is either “knocked-out” or overactive and plans to cross them with models of Alzheimer’s disease, Parkinson’s disease and ALS to see if it can prevent neurodegeneration. He is also actively screening for small molecule compounds that can elevate this microRNA and promote neuronal survival.
The research was funded by the National Institutes of Health. Study co-authors were Adam J. Kole, a graduate student in Deshmukh’s lab; Vijay Swahari, research technician; and Scott M. Hammond, PhD, associate professor of cell and developmental biology.

[Six Foot Three]

Originally Posted by baystater

I've see most of these diseases near their ending stages with the exception of ALS (seen fresh stokes as well.)

ALS is such a puzzle as they still are mostly clueless about what the cause of it is. That being said there has been some headway as clues are starting to surface e.g. an immune system component found in the CNS called the ''Microglia'' has gone array as well as some genetic component with the SOD-1 genes (protect neurons) possibly being defective and also the protein TDP-43 forming mutated clumps possibly being implicated. Anyway i just dig biology especially about incurable diseases and also antiaging and so thanks for the thread here Brian

[Brian.Pearson]

Originally Posted by 6 Foot 3

ALS is such a puzzle as they still are mostly clueless about what the cause of it is. That being said there has been some headway as clues are starting to surface e.g. an immune system component found in the CNS called the ''Microglia'' has gone array as well as some genetic component with the SOD-1 genes (protect neurons) possibly being defective and also the protein TDP-43 forming mutated clumps possibly being implicated. Anyway i just dig biology especially about incurable diseases and also antiaging and so thanks for the thread here Brian

Me, too. I recently heard about alpha lipoic acid and had ordered it as a supplement. I have both the ala and the r-ala. Maybe I'll last a little longer...