So what’s the catch?
For one, iPSCs can take months to make and the process is expensive. Furthermore, reverting cells back to a stem cell state wipes out their history, which is sometimes useful for studying disease progression.
In essence, iPSCs are the middlemen between one cell type and another. What if we could simply take out the middleman altogether?
Scientists at Hollings Cancer Center at the Medical University of South Carolina have found that human lung cancer cells resist dying by controlling parts of the aging process, in results published online May 10th in the Journal of Biological Chemistry. The discovery could help us better understand aging and eventually could lead to new treatments for cancer.
Cancer becomes more common as people get older, but scientists are still searching for answers about why this happens. At Hollings Cancer Center, research into the connections between aging and cancer is led by Besim Ogretmen, Ph.D., SmartState Endowed Chair in Lipidomics and Drug Discovery. Ogretmen’s team found that cancer cells have specific ways to resist dying the way normal cells do. They do so by protecting the tips of their chromosomes, which hold our DNA, from age-related damage.
Ogretmen studies how cancer cells are different than normal cells to understand how cancer grows and spreads in the body. His work is part of an $8.9 million program project grant to research how alterations of lipid metabolism affect cancer therapy. The grant is helping fund a clinical trial of an anticancer medicine to inhibit cellular signaling that helps cancer survive. The drug was found to be useful against cancer in the research reported in the group’s new paper.
In the longer term, our descendants may face even more existential decisions (provided the machines allow them to make them). How might they organise society in a world in which few people can do anything that is obviously economically productive? The world might become techno-feudal, with an owning elite hiring great numbers of cheap human servants not for their value, but for the pleasure of domination. People might instead share the abundance more equally, with all enjoying the civilised leisure that was once the province of the very few. Ours is the first civilisation to view work as the highest calling. Maybe that strange prejudice will need to be discarded.
How do you organise a society in which few people do anything economically productive?
“I am extremely excited about the research involved in the current Scientific Reports article,” said Joseph I. Shapiro, M.D., senior author and dean of the Joan C. Edwards School of Medicine. “I believe that our team has not only implicated the NAKL discovered by our colleague, Dr. Zijian Xie, in the aging process but identified a novel therapeutic target as well as a specific pharmacological strategy to actually slow the aging process. Although it will be some time before we can test these concepts in human subjects, I am cautiously optimistic that clinical therapeutics will ultimately result.”
The team’s extensive year-long study first focused on aging mice who were given a western diet to stimulate oxidant stress to antagonize the NAKL. The western diet increased the functional and structural evidence for aging; however, the introduction of pNaKtide slowed these changes in the mice. The same results were then replicated when human dermal fibroblasts were exposed to different types of oxidant stress in vitro by stimulating the NAKL, increasing expression of senescence markers, and causing cell injury. With pNaKtide treatment, the researchers demonstrated that the negative attributes associated with aging were significantly dampened.
“Our data clearly suggest that the Na/K-ATPase oxidant amplification loop is intimately involved in the aging process and, if confirmed in human studies, might ultimately serve as a therapeutic target,” said first author Komal Sodhi, M.D., an associate professor of surgery and biomedical sciences at the Joan C. Edwards School of Medicine. “If the pNaKtide can be safely used in humans, it might be possible to study the applicability of that specific agent to the problem of clinical aging.”
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Google, Facebook, Twitter and Microsoft formed the Global Internet Forum to Counter Terrorism last year to prevent terrorists from exploiting their services.
A remarkable new study has successfully used the CRISPR-Cas9 gene editing technique to edit a specific gene in mice engineered to have fragile X syndrome (FXS), a single-gene disorder often related to autism. The single gene edit in the live mice resulted in significant improvements in repetitive and obsessive behaviors, making this the first time gene editing has been used to effectively target behavioral symptoms related to autism spectrum disorder (ASD).
FXS is a genetic disorder associated with intellectual disability, seizures and exaggerated repetitive behavior. Previous studies have shown that the repetitive behaviors associated with FXS are related to a specific excitatory receptor in the brain that, when dysregulated, causes exaggerated signaling between cells.
The CRISPR technique homes in on the gene that controls that excitatory receptor, the metabotropic glutamate receptor 5 (mGluR5), and essentially disables it, dampening the excessive signaling the corresponds with repetitive behaviors. In mice treated with the new system, obsessive digging behavior was reduced by 30 percent and repetitive leaping actions dropped by 70 percent.
For the first time ever researchers have had a breakthrough in creating a cocktail of drugs that caused new neurons to grow in the brains of mice.
In my last article I gave a detailed account on the debate of neurogenesis. While some neuroscientists claim that neurogenesis takes place within the adult mammalian human brain other researchers contest that idea claiming that new neurons stop developing at a very young age. Whichever side of the debate you are on one thing remains certain, that there are neurological diseases that leave negative impacts on cognitive function. This has left researchers looking for various ways to treat Alzheimer’s, Parkinson’s, and other brain damage.
While the brain is incredibly complex and past research has failed to offer much hope for Alzheimer’s disease, Hongkui Deng at Paking University Health Science Center in China may finally be able to change that.
For the first time ever researchers have had a breakthrough in creating a cocktail of drugs that caused new neurons to grow in the brains of mice.
What this cocktail does when injected into the brain is it hijacks the astrocytes into behaving like new neurons. This is significant for a number of reasons. One important detail about astrocyte cells is that they can survive after a stroke while regular neurons die. Another important detail is that there are 10 times more astrocytes in the brain than neurons. That means that there are 1 trillion glia cells within the brain. So not only are they more resilient than neurons they outnumber them too.
Deng and his team of researchers have found that when the cocktail is injected into the brains of mice that it effectively gives the cell a new identity by erasing its old one and giving it a new one. Not only did the cells change shape but they showed change in gene activity too.
The results were substantial. While it remains speculative as to how closely the cells resemble normal neurons, around 80 to 90 per cent of the astrocytes started to resemble neurons and even mimicked their behavior by electrical signals the same way regular neurons do.
“They are unlikely to be a 100 percent match” Deng stated. “But the treatment was safe and none of the mice developed any health problems”.
Matthew Grubb at King’s College London states that “if it holds up it’s absolutely amazing, and has a lot of potential applications and exciting consequences. If you’ve got a degenerating brain, for example in Alzheimer’s disease, and you could get the brain to regrow neurons itself, it would be a huge step forward.”
The next step for the researchers will be to test the cocktail in mice that have had a stroke. The hope is that the cocktail will cause the astrocytes to behave as neurons and help the mice recover.
While Grubb admits it is difficult to predict the effects of the treatment in humans, if it works in mice then it offers new hope for those who suffer from neurodegenerative diseases such as Alzheimer’s or Parkinson’s. While it is unlikely to bring back lost memories Grubb thinks it might restore the ability to create new ones.
Even though the research is promising there still remain challenges as Roger Barker at the University of Cambridge points out. The sheer numbers of cells lost in a neurodegenerative disease is something to consider. “In Parkinson’s, a quarter of a million cells are lost from either side of the brain. Currently Barker is conducting clinical trials of implants of brain tissue taken from aborted fetuses as a treatment for Parkinson’s.
Another challenge is to distinguish the types of neurons the drugs will make. As Grubb points out, if you make too many of the type of neurons that excites their neighbors you end up triggering epilepsy. Grubb also points out that different brain disorders effects different types of neurons which is another reason why we need to be capable of distinguishing them. The neurons that die from Parkinson’s are the neurons that create the chemical dopamine for example.
Another example is balancing the risks for rewards. As Grubb points out “you’d have to have extremely good control over what cells you’re programming, where they’re going to go, and which cells they’ll connect to. If the treatment were to be used to boost grey matter, for example, this could provide a way to improve skills like memory. However, too much grey matter has been linked to causing people to be being easily distracted.
While the research is definitely groundbreaking it is still in its early stages. Hopefully in the near future it will offer treatments to those who need them.
Buzz Aldrin wants people to know that he has some cool new ideas about how to get to the moon — not just because they’re cool, but also because they show his mind is working.
“That’s not an inactive, incapacitated, dependent mind,” the 88-year-old Aldrin, who became one of the first humans to walk on the moon during 1969’s Apollo 11 mission, told me today during a wide-ranging telephone interview.
