Saturday December 14, 2019

Checkpoint Protein (CHK2) Inhibitor Drug to Protect Women’s Infertility Post Cancer Treatments

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Sep 02, 2017: An existing drug may one day protect premenopausal women from infertility that commonly follows cancer treatments, new research has found.

Women who are treated for cancer with radiation or certain chemotherapy drugs are commonly rendered sterile.

Women are born with a lifetime reserve of oocytes, or immature eggs, but those oocytes are among the most sensitive cells in the body and may be wiped out by such cancer treatments.

The new findings, published in the journal Genetics, raises hope of curbing infertility from cancer treatment.

The study builds on his 2014 research that identified a so-called checkpoint protein (CHK2) that becomes activated when oocytes are damaged by radiation.

Checkpoint protein functions in a pathway that eliminates oocytes with DNA damage, a natural function to protect against giving birth to offspring bearing new mutations.

When the researchers irradiated mice lacking the CHK2 gene, the oocytes survived, eventually repaired the DNA damage, and the mice gave birth to healthy pups.

Also Read: Treatment with Uterine Fibroids helps to restore Fertility in Women

The new study explored whether the checkpoint 2 pathway could be chemically inhibited.

“It turns out there were pre-existing CHK2 inhibitor drugs that were developed, ironically enough, for cancer treatment, but they turned out not to be very useful for treating cancer,” said study senior author John Schimenti, Professor at Cornell University in New York.

“By giving mice the inhibitor drug, a small molecule, it essentially mimicked the knockout of the checkpoint gene,” first author Vera Rinaldi, a graduate student in Schimenti’s lab, said.

By inhibiting the checkpoint pathway, the oocytes were not killed by radiation and remained fertile, enabling birth of normal pups, the study said.

“While humans and mice have different physiologies, and there is much work to be done to determine safe and effective dosages for people, it is clear that we have the proof of principle for this approach,” Schimenti said. (IANS)

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Development of Alzheimer’s Disease Not Totally Linked to Genetics: Study

The research team analyzed the gene sequence and the biological age of the body's cells from blood

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Genetics
With additional funding, researchers could further explore the interaction between Genetics and environment in the development of Alzheimer's disease and the impact of environmental factors in delaying the onset of this disorder. Pixabay

The colour of our eyes or the straightness of our hair is linked to our DNA, but the development of Alzheimer’s disease isn’t exclusively linked to Genetics, suggest new research.

In the first study published about Alzheimer’s disease among identical triplets, researchers found that despite sharing the same DNA, two of the triplets developed Alzheimer’s while one did not.

The two triplets that developed Alzheimer’s were diagnosed in their mid-70s, said the paper published in the journal Brain.

“These findings show that your genetic code doesn’t dictate whether you are guaranteed to develop Alzheimer’s,” said Dr Morris Freedman, head of neurology at Baycrest Centre for Geriatric Care.

“There is hope for people who have a strong family history of dementia since there are other factors, whether it’s the environment or lifestyle, we don’t know what it is, which could either protect against or accelerate dementia.”

All three, 85-year-old siblings had hypertension, but the two with Alzheimer’s had long-standing, obsessive-compulsive behaviour.

The research team analyzed the gene sequence and the biological age of the body’s cells from blood that was taken from each of the triplets, as well as the children of one of the triplet’s with Alzheimer’s.

Genetics
The colour of our eyes or the straightness of our hair is linked to our DNA, but the development of Alzheimer’s disease isn’t exclusively linked to Genetics, suggest new research. Pixabay

Among the children, one developed early onset Alzheimer’s disease at age 50 and the other did not report signs of dementia.

The research team also discovered that although the triplets were octogenarians at the time of the study, the biological age of their cells was six to ten years younger than their chronological age.

In contrast, one of the triplet’s children, who developed early onset Alzheimer’s, had a biological age that was nine years older than the chronological age.

The other child, who did not have dementia, of the same triplet showed a biological age that was close to their actual age.

Genetic
Your Genetic code doesn’t dictate whether you are guaranteed to develop Alzheimer’s Disease. Pixabay

“The latest genetics research is finding that the DNA we die with isn’t necessarily what we received as a baby, which could relate to why two of the triplets developed Alzheimer’s and one didn’t,” says Dr. Ekaterina Rogaeva, senior author on the paper and researcher at the University of Toronto’s Tanz Centre for Research in Neurodegenerative Diseases.

“As we age, our DNA ages with us and as a result, some cells could mutate and change over time”.

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With additional funding, researchers could further explore the interaction between genetics and environment in the development of Alzheimer’s disease and the impact of environmental factors in delaying the onset of this disorder. (IANS)