Adult Neurogenesis

Friday, November 27, 2009

what is adult neurogensis?
Adult neurogenesis is the formation of new neurons in adult brain. It was a prevailing belief that mature brain can not produce new neurons.

A number of reasons behind this belief, includes
- limited capacity of self-reparing in mammal brain and spinal cord.
- structural consistency of mammalian brain throughout the life with an unchanging number of neurons of about 100 billion.

Besides, it is very difficult to imagine how new neurons could develop and integrate successfully into the mature brain structure. However ,due to scientist's arduous search for unknown and enormous technical development, many evidence are found regarding adult neurogenesis and it is now widely accepted by the scientific community.

Where does adult neurogenesis occur?
Most cells in the brain are formed during embryonic and early post-natal period while new neurons are also generated throughout life and are added to at least two areas of the brain: the hippocampus ( involved in certain types of learning and memory) and the olfactory bulb ( involved in the sense of smell). New neurons are spawned from the division of neural precursor cells — cells that have the potential to become neurons or support cells.


click on image to view the full image....


New hippocampal neurons are generated by neural precursors located in the hippocampus, in a region known as the subgranular zone. In contrast, new olfactory neurons arise from neural precursors located outside of the olfactory system, in a region known as the subventricular zone of the lateral ventricle. These cells migrate to the olfactory bulb through a tract known as the rostral migratory stream.

What are the functional significance of newly synthesized neurons?
Experimental studies suggest that new neurons integrate into the circuitry of the brain and actively participate in its functions. The hippocampus is known to play a critical role in learning and memory and many scientists have hypothesized that newly generated neurons within the hippocampus contribute to these processes. Although currently limited, there is support for this hypothesis. For instance, conditions that impair adult neurogenesis, such as stress, also impair learning. In contrast, conditions that promote the generation of new neurons, such a physical exercise , often are associated with improved memory and learning.

Studies have shown that the beneficial effect of many antidepressant are diminished when neurogenesis is blocked. Again many therapies and medication that are used to treat patients suffering from depression can cause an increase in hippocampal neurogenesis .So clearly, there is a link between adult neurogenesis and neurological disorder. We can expect, in near future neurological disorder can be cured by manipulating neurogenesis, though its still very much impossible.

Many studies have shown that neurogenesis is stimulated in the mammalian brain in response to injury and disease. Although this injury-induced neurogenesis does not lead to recovery, many scientists believe it represents brain's attempt to mend itself. Now, if we can understand the mechanism of neurogenesis and the integration of new neurons to nervous system its may be possible to cure or give life to a patient having severe brain stroke !!!

Once it was thought, once you were grown all you could do was watch your brain cells die. But things are changed. The discovery of life-long neurogenesis in humans has redefined the understanding of the brain and spinal cord. Lots of expectation has already been arisen with this discovery. We can suddenly hope that new strategies will be developed to treat injuries and diseases of the brain and spinal cord in future.

Source:

How new strain of influenza viruses evolve ?

Saturday, September 5, 2009

Whenever a new version of virus evolves , there's a chance that it'll become pandemic. Its because human does not have immuno resistance against that new strain. However, the interesting Ques. is how these new strains evolve?

New strain of virus ( like " Nobel H1N1" ) can be emerged via two basic processes.They r -
1. Antigenic Shift
2. Antigenic Drift

Antigenic shift is the process by which at least two different strains of a virus (or different viruses), especially influenza, combine to form a new subtype having a mixture of the surface antigens of the two original strains. The term antigenic shiftis more often applied specifically (but is not limited) to the influenza. Antigenetic shift is a specific case of reassortment or viral shift that confers a phenotypic change.

Genomes of influenza virus consist of 8 distinct segments of RNA . These segments act like mini-chromosomes, and each time a flu virus is assembled, it requires one copy of each segment. If a single host (a human, a chicken, or other animal) is infected by two different strains of the influenza virus, then it is possible that new assembled viral particles will be created from segments whose origin is mixed, some coming from one strain and some coming from another. The new reassortant strain will share properties of both of its parental lineages.

click on the image to view it larger


Another term Antigenic drift is completely diferent and should not be confused with Antigenic shift. Random mutations in the genes of a virus drives antigenic drift that changes the antigens of the virus. As these changes accumulate it may help the virus to evade the immune system since antigens are what the immune system recognizes.

Thus a new strain can evolve by the genetic changes in viral genome... !

Reference:
http://en.wikipedia.org/wiki/Antigenic_drift
http://en.wikipedia.org/wiki/Antigenic_shift

Nobel H1N1 Swine influenza virus in brief

Wednesday, September 2, 2009

Introduction
Swine influenza virus is actually a virus of pigs and its commom thoughout pig population worldwide. Transmission of this virus from pigs to human is rare and it usually can not pass from human to human. But early in this year (2009), a new strain of influenza virus is found in human (a zoonosis) which was thought to be come from pigs and its capable of spreading from human to human. This virus is classified under influenza A, subtype H1N1, generally known as the swine flu virus or "nobel H1N1"

What does H1N1 mean actually?
There r 3 genera of influenza virus that cause human flu. Those r Influenza A, B and C. Influeza A is the most common cause of seasonal flu,but also there are some other strain of influenza A those are endemic in pigs and birds. Influenza A virus strains are categorized according to two proteins found on the surface of the virus: hemagglutinin (H) and neuraminidase (N). All influenza A viruses contain hemagglutinin and neuraminidase, but the structures of these proteins differ from strain to strain, due to rapid genetic mutation in the viral genome. Influenza A virus strains are assigned an H number and an N number based on which forms of these two proteins the strain contains. 3 H and 2 N subtypes r common in human.

Origin
The new strain was initially described as an apparent reassortment (mixing of the genetic materials of two or more viruses) of at least four strains of influenza A virus subtype H1N1, including one strain endemic in humans, one endemic in birds, and two endemic in swine. Subsequent analysis suggested it was a reassortment of just two strains, both found in swine. Although initial reports identified the new strain as swine influenza (i.e., a zoonosis originating in swine), its origin is still not clear.



Who r in risk?
Those who have lower immuno resistance ,such as children, HIV positives r very much susceptible for this virus.The U.S. Centers for Disease Control and Prevention (CDC) noted that although this was a very serious virus, cases worldwide were usually mild, and most hospitalizations and deaths had been of persons that also had underlying conditions such as asthma, diabetes, obesity, heart disease, or a weakened immune system.

Vaccination
Vaccines are available for different kinds of swine flu. Although the current trivalent influenza vaccine is unlikely to provide protection against the new 2009 H1N1 strain,vaccines against the new strain are being developed and could be ready as early as November 2009. Besides, ayurvedic experts said, tulsi pata( a herb) provide a little bit resistance against swine flu as well as any other seasonal flu. But if the new virus mutated futher ,it could become more virulent and less susceptible to any new vaccines.

reference:

Cancer cells and embryonic stem cells r immortal. How they escape death ?

Monday, June 15, 2009

In 1961 ,Dr, Leonard Hayflick discovered that when cells are taken from the body and grown in tissue culture on a laboratory dish, there is a limit to how long the cell line lives . After about 50 (the num varies with the kind of tissue) divisions, the aging cell line dies. Its known as Hayflick limit. This Hayflick limit has puzzled developmental biologists for decades. What causes the cells, after so many successful divisions, to abruptly break down ? How does a cell know its time is up?


But scientist now know all the answers !!!

The secret to immortality proved to be a short tag of DNA attached on the tips of the cell's chromosomes,known as telomere. This segment of DNA plays a key role in cell division. The telomere provides a place for the cell's DNA-copying machinery to latch onto the chromosome when the time comes for the chromosomal DNA to be copied into daughter chromosomes. However, every time the machinery attaches, the short bit of the telomere where the machinery sits down on the DNA is not itself copied, so the telomere gets a little shorter each time the cell divides. When the telomere reaches a minimal length after some 50 divisions, the cell can no longer replicate its DNA and lapses into senescence.





So, why Cancer and ESC cells are immortal ?

All cells possess a gene, known as the telomerase gene, which can add DNA back to the tip of telomeres. In almost all cells this gene is turned off early in development. If somehow, this gene is turned on then the cell become a cancer cell.

Embryonic Stem Cells also have the telomerase activity. But when they differentiate into other specialized cells they lose their telomerase activity ,as well as immortality. A few, however, are set aside, protected from the influences that trigger differentiation and shutting down of the telomerase gene. Called germ line cells, these embryonic stem cells have a fully functional telomerase gene and continue to divide, producing eggs and sperm that in their turn produce more stem cells in the next generation.


reference :

Giving Birth of extincted creature !!! possible or not?

Wednesday, June 3, 2009

The recipe for making any creature is wriitten in its DNA. If so,then its very much possible to regenerate an extincted organism from its DNA (when the complete DNA sequence of that organism is known).


Creating a living, breathing creature from a genome sequence that exists only in a computer's memory is not possible right now. But someone someday is sure to try it, predicts Stephan Schuster, a molecular biologist at Pennsylvania State University. It is only going to be possible with creatures for which we can retrieve a complete genome sequence. Without this, there is no chance,he added.

Usually when a creature dies, the DNA in any flesh left untouched is soon destroyed as it is attacked by sunshine and bacteria.There are, however, some circumstances in which DNA can be preserved. If your specimen froze to death in an icy wasteland such as Siberia, or snuffed it in a dark cave or a really dry region, for instance, then the probability of finding some intact stretches of DNA is much higher.

Even in ideal conditions, though, no genetic information is likely to survive more than a million years - so dinosaurs are out. "It's really only worth studying specimens that are less than 100,000 years old," says Schuster.

The genomes of several extinct species are already being sequenced, but turning these into living creatures will not be easy . "It's hard to say that something will never ever be possible," says Svante Pääbo of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, "but it would require technologies so far removed from what we currently have that I cannot imagine how it would be done."

But 50 years ago, who would have believed we would now be able to read the instructions for making humans, fix inherited diseases, clone mammals and be close to creating artificial life?

So, its for sure , oneday something like this will be done !!!
Its all about the fascinating science of Genetic Engineering and no one knows where to stop thinking !!!



Reference:
http://www.newscientist.com

Y chromosome is minimizing its length but will not be extincted !!!

Thursday, May 28, 2009

All chromosomes in the nucleus come in pairs – except the Y chromosome. Each member of a chromosomal pair depends on its mate for genetic repair through sexual recombination. When one half suffers a genetic injury, it can discard the mutated gene and replace it with a normal copy drawn from the other member of the pair. But the Y has no sexual 'partner' with which to swap out defective genes.


However,Researchers from Whitehead Institute for Biomedical Research and Washington University School of Medicine suggested that Y chromosome includes a large number of genes arranged in pairs along this single chromosome in ways that may allow the Y to mimic the paired chromosome structure of the rest of the genome.

"Genes constantly are being bombarded with little injuries – mutations. Mutations can either be beneficial or detrimental, but they are far more often detrimental," said lead researcher David Page. "On the Y, detrimental mutations cannot be discarded."

There's no question that this inability to discard has cost the Y hundreds of genes over time. Many of the chromosome's genes either have weakened or died out altogether. Sexual recombination is a card game the Y just can't win. But this new research suggests it doesn't always need to. For critical genes, it swaps with itself.

Rather than swapping DNA with the X, the Y may exchange DNA with itself, in a recombination process mediated by the palindromes. The palindromes contain genes, so in effect the Y could be able to repair itself, replacing bad sequence with good, suggested by David Page.




"This study shows that the Y chromosome has become very efficient at preserving its important genes," said co-lead investigator Richard K Wilson. "It's found different ways to do the things that chromosomes must do to evolve, survive and thrive."

However, not all scientists r convincened by this! As Mark Jobling points out, the evolutionary cost of this mechanism is very high to occur !!!

reference:
http://genome.wellcome.ac.uk

Men on the road to extinction !!!

Monday, May 25, 2009

Professor Jennifer Graves, a leading researcher in human sex chromosome from australia, claims the male Y chromosome was dying and could run out within the next 5 million years.

While at the annual outreach public lecture at the Royal College of Surgeons in Ireland, Graves said,"You need a Y chromosome to be male." "Three hundred million years ago, the Y chromosome had about 1,400 genes on it, and now it's only got 45 left, so, at this rate, we're going to run out of genes on the Y chromosome in about five million years. The Y chromosome is dying and the big question is what happens then," she added.

 The male Y chromosome has a gene - SRY. SRY switches on the development of testes and pumps out male hormones that determine maleness. She said it was not known what would happen once the Y chromosome disappeared. 




"Humans can't become parthenogenetic, like some lizards, because several vital genes must come from the male," she said."But the good news is certain rodent species - the mole voles of Eastern Europe and the country rats of Japan - have no Y chromosome and no SRY gene. 

"Yet there are still plenty of healthy male mole voles and country rats running around. Some other gene must have taken over the job and we'd like to know what that gene is," she added.


Earliar in 2003,Brian sykes said, time will come when Y chromosome will cease to exist. Because,Over each replication hangs the threat of a random genetic mutation, which can be handed down to the next generation. Unlike other chromosomes, which are paired and can exchange genetic material with each other, the lowly Y has no duplicate from which to seek repair. Slowly but surely, Y chromosomes throughout the world are being pounded into submission.


Stem cells have the ability to grow into many other types of cell. if so, why its still not possible to grow a functional organ in the lab?

Friday, May 22, 2009

 Let's consider all of the things you would need to make an organ - say, a kidney - in a lab dish.

  1. First, you need to obtain a type of stem cell that can ultimately become a kidney. Would this be an embryonic stem cell? A fetal stem cell? Will an adult stem cell do the job? How do you know? Where will you get the cells?

  2. Next, you have to coax the stem cells to grow and divide in a lab dish. Which nutrients will help them grow? Do they need other types of cells around to encourage them to divide? If so, can you obtain them?

  3. After you have enough stem cells, you must simulate the physical environment required for them to differentiate into a functional kidney. How do you make the cells begin differentiating? Can you simulate the physical environment they need? Can you create a physical scaffold, or foundation, upon which the cells can shape themselves into a kidney? How will you help the developing kidney grow blood vessels to supply oxygen and nutrients to cells on the interior?

Scientists are still years away from growing whole human organs in lab dishes - but not for lack of trying. Research groups around the world have convinced various types of stem cells to grow, divide and even differentiate in lab dishes. Most of this research is performed in stem cells obtained from other organisms, such as mice, rats and frogs.

The final step, creating a functional organ out of differentiating stem cells, is more challenging. Obstacles to success include the problem of delivering oxygen and nutrients to cells on the inside of the organ, as well as creating physical scaffolds upon which to grow and differentiate cells.


reference:

http://learn.genetics.utah.edu

 
 
 
 
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