Researchers were wondering from ages as to what could be the actual cause of Huntington’s disease which causes involuntary jerky body movements disabling the victim to exhibit physical and mental coordination. The awkward bodily momentum gradually worsens after the initial unsteady gait putting the victim in jeopardy. Parental inheritance being the focal reason, this disease is hard to prevent and has been affecting millions of people globally without a documented cure. However, the available treatments reduce the severity of the symptoms and aid the victim in lessening the care giving requirements.

To enhance the quality of life of the global populace affected with Huntington’s disease, researchers are looking forward to get core advancement in finding an explicit medical solution. However, the extensive research to find the root cause of Huntington’s disease has enabled the researchers to get a key which can be a potential advancement in finding a generic solution to lessen the severity of the ailment. It is established that a mutant of the Huntington (mHTT) protein is the fundamental cause of the disease though the researchers are still unclear as to how it disturbs the brain cells’ function. As per the established findings of late, mHTT vitiates the cellular transport process adding to the neurotoxicity eventually resulting in loss of neurons.

Caused by an extended CAG repeat in the Huntington (HTT) gene, this neurodegenerative disease with mHTT plays pivotal role in disrupting the transport system of a cell which normally requires mobilizing multiple elements from its nucleus to the other parts and vice-versa. It has been pragmatically realized that mHTT creates aggregates in the central operations area that is in the nucleus preventing it from passing through the nuclear pores.  This pile up in the mHTT following the stagnation in the nuclear passages kills the brain cells by shutting them down.

The new fact discovered can drive the researchers to find out new ways to fix the cellular traffic jams there by aiding the process of finding new treatment methodologies for the Huntington’s disease. Although it is a fact that this step towards an advanced research in finding the cause for the disease is in the initial stage, the researchers are excited with their discovery as these findings are the stepping stones in conquering the Huntington’s disease along with encouraging the search for new therapeutic modules.

Biotech companies and pharmacy companies are looking forward to dwell on this very concept to capitalize it and bring into existence various therapies for biological processes. Hope they get abundant clues to prove the fact that early birds get quick worms in the course of their research. Ultimately, it is the millions of people who are affected with the Huntington’s disease who get the best of the research.

The post Cellular Traffic Jam Is The Culprit Behind Huntington’s Disease appeared first on Stem Cell Banking Guide and Pregnancy Tips For New Parents.

This is the story of Doug Oliver, who suffered from macular degeneration or progressive blindness for more than two years. His medical team conducted a stem cell treatment on him and now he has recovered his eyesight and is leading a healthy life.

Doug started losing his vision at the age of 32. When consulted with doctors, they told him that this was the result of macular degeneration and he would gradually lose his vision. Doctors did not give him any hope and said nothing could be done to regain his sight.

To make the situation worse for him, he met with an accident after the diagnosis, which made his stand in front of another devastating news. He might lose his vision completely. Some tests were done on him that revealed his vision was as 20/2000 in the left eye and 20/400 in the right eye.

However, having found out about his condition, Doug was not willing to give up. He was not ready to succumb to the prediction that his sight could not be cured. So, he started screening latest clinical studies, databases, and trials related to macular degeneration. This was the time when Doug discovered Dr. Jeffrey Weiss’s clinical trial with stem cells in order to treat macular degeneration.

Doug enrolled himself in the Florida-based trial in 2015. And only after two days of stem cell therapy, he started to feel a difference in his vision. The stem cell therapy involved extracting his own stem cells from his marrow of the hip bone. The stem cells then were injected directly into both of his retinas. Two days later, his vision showed an improvement to 20/40 in his left eye and 20/30 in the right eye.

The joy of seeing the world again in its full glory was evident in his confession that he made while he was going back home. He said, “I could see the boats and the little wake lines that you see from 30,000 feet. I acted like a 6-year-old and loved it.”[1]

Doug was an IT specialist and a social policy consultant. His job demanded a lot of traveling by car. During one of those drives, he realized that his vision was not as same as before. Moreover, the accident cost him his driving license as well, which eventually led him to lose his job. He was not only going through physical issues but also through a mental turmoil. An active person like him needed to rely on a monthly disability check. But stem cells helped him bounce back and how!

Doug has not only got his vision back, but he also gained his position back in the community. He said, “I went back to the DMV and got my license in Tennessee in December.”[2] He is currently in talks with Lamar Alexander, the Senate Health Committee Chairman, so his can share his experience and story with others. Doug’s story may also play a crucial role in passing the 21st Century Cures Act, which focuses on the advanced regenerative therapy and the required funding for clinical trials, similar to one he was a part of.

The post Stories of Hope: Cured Of Blindness: A Stem Cell Therapy Story appeared first on Stem Cell Banking Guide and Pregnancy Tips For New Parents.

Aging is a natural process that no one can deny. But how about a treatment that will not only keep your muscles flexible during the normal aging process, but also treat various muscle wasting diseases? Well, this is no more a mere concept. The Stanford University School of Medicine researchers have discovered that stem cells, present in the muscle tissues, can prevent tissue scarring, clinically termed as fibrosis.

Thomas Rando, who lead the study, said, “Fibrosis occurs in many degenerative diseases and also in normal aging,” he added, “It negatively impacts muscle regeneration by altering the stem cell niche and inhibiting the stem cell function. In addition, as more scarring occurs, muscles become stiff and can’t contract and relax smoothly.”

The team tried to understand how normal muscle tissues regenerate under usual circumstances and at the same time how they respond to injuries. During the research, they concentrated on fibro-adipogenic progenitors (FAPs), the stem cells that reside in the muscle and build the desired connective tissue structure to support muscle regeneration.

The findings of the research are quite amazing. Not only had they discovered that the stem cells in the muscle have the ability to respond to aging, injuries or diseases, but also they can prevent fibrosis.

The scientists studied PDGFR alpha (PDGFRa), a protein found on the surface of FAPs.  The structure and function of the PDGFRa protein is quite intriguing. It straddles the cell membrane. The outer part of the protein functions as a landing area for any external factors that encourage the FAP cells to divide. The inner portion helps to pass on the external signal inside. If the response is somehow over-enthusiastic, it may lead to fibrosis. So, a balanced response on the stem cell’s part is required for an optimum result.

The study showed that the muscle-embedded stem cells can police themselves to get the optimum response. Rando pointed out, “We’ve found that the cells actively regulate the production of the inhibitory form of the protein, which is very surprising. If they make less, the degree of fibrosis increases; if they make more, it decreases.”

The normal version of PDGFRa protein instructs the FAPs to divide and grow, which is ideal if FAPs try to repair any tissue damage. However, excessive growth may lead to fibrosis. In order to avoid it, FAPs build a truncated version of PDGFRa protein that orders the cells to prevent tissue scarring by restricting any further division.

The research team figured out that the stem cells create a shortened version of the protein, which is not there in the interior portion. The shortened version of the protein hides the external growth signals away from the larger version of the protein. The cells grow the ability to create the shortened form of the protein by identifying and implementing a series of nucleotides. The nucleotide code then instructs the cell’s messenger RNA to set up a shorter signal. Consequently, the protein gets truncated.

The researchers forced the FAPs to build the shortened version of the protein in a mouse model. Followed by the process, both young and old mice showed less scarring. The team is soon to test this approach for muscle wasting diseases like muscular dystrophy in a similar mouse model. We will certainly keep you updated on the findings. Stay tuned!

The post Stem Cells Have a Neat Trick to Prevent Tissue Scarring appeared first on Stem Cell Banking Guide and Pregnancy Tips For New Parents.

Have you ever thought about bringing back the memories of those who are currently fighting to remember? Imagine if you could cure about 4 million Indians living with Alzheimer’s disease (AD) that is expected to triple by 2050. It’s not a small task by any means.

Recently, Hong Kong’s South China Morning Post newspaper published a scientific study claiming to have reached significant progress in reversing memory loss using cell-based treatment in mice with Alzheimer’s. A group of Chinese scientists chose to produce in the brains of the mouse model AD patients, a typically “lost” of dysfunctional nerve cell. Living in the area near the bottom of the brain, it is known as the basal forebrain cholinergic neuron that helps process functions like leaning and attention. Memory function could be restored by replacing those dysfunctional nerve cells in the AD mice with healthy nerve cells extracted from stem cells.

So how did they do it?

Initially, the research team used a methodology to generate these specific types of nerve cells extracted from both the human embryonic stem cells and the mouse in a petri dish. Their first step was successful, meaning that the newly produced nerve cells imbibed within them the required markers for cholinergic neurons in order to function properly. This essentially suggests that the nerve cells would be able to send the right signals to the other nerve cells.

In order to test the functionality of the nerve cells, the subsequent step comprised of transplanting the progenitor cells, which are specialised in developing into adult nerve cells, into the brains of the mouse models of AD. Most of the transplanted mouse progenitor cells endured and developed into cholinergic nerve cells. They, in turn, were able to perform in sync with the original mouse nerve cells. On the other hand, the human progenitor cells, when transplanted into the same area of the brain, the majority were not able to survive as expected. However, the breakthrough was that the ones that did make it through started to function as cholinergic neurons.

Hence, could memory be improved in these forgetful mice was the final question that the research team needed to address.

In order to measure up the memories of AD mice that had been given the mouse or human cholinergic progenitor cells to AD mice that received no treatment and to healthy normal mice, the group put together a memory test. The model mice were taught to locate a hidden platform in a circular pool of water. Substantiating the prognosis of the study, the test showed that the untreated AD mice had difficulty locating the hidden platform. In subsequent tests, they could not even recall its location at all. In comparison to them, the group of treated AD mice performed significantly better and were able to retain directions and find the location in multiple trials. This test implied that the transplanted nerve cells enhanced their capability to absorb tasks and recollect memories.

The study still at very early stages was able to establish the foundation of a possible method to retrogressive memory loss in Alzheimer’s disease via substituting cholinergic nerve cells in the basal forebrain area of the brain. However, the study’s senior author, Naihe Jing, cautioned everyone to not get ahead of themselves and said, “Mice are still very different from humans, so the results on mice do not guarantee the same success on human patients. Our next step is to test the method on primates. It will probably be a long time before clinical trials can be carried out on human volunteers.”

Dr. Naihe Jing additionally described the precautions that his team were taking in order to test the safety of their embryonic stem cell-based therapy.

“We used human embryonic stem cells because this method will eventually be used on humans. If the human neurons can get a footing and grow in the brain of a mouse, the chance is high the effect will be even better on a human host. The biggest concern of this development is safety. We were afraid that the transplanted cells would mutate to other types of neurons or even cause brain tumours. We have been improving the technology and making close observation of the mice for more than seven years. So far no mutation or cancerous development has been detected.”

The post Could We Reverse Alzheimer’s Disease With Stem Cells? appeared first on Stem Cell Banking Guide and Pregnancy Tips For New Parents.