Posts tagged degenerative diseases
Articles and news from the latest research reports.
Peptides helping researchers in search for Parkinson’s disease treatment
Australian researchers have taken the first step in using bioactive peptides as the building blocks to help ‘build a new brain’ to treat degenerative brain disease.
Deakin University biomedical scientist Dr Richard Williams is working in a team with Dr David Nisbet from the Australian National University and Dr Clare Parish at the Florey Neuroscience Institute to develop a way to repair the damaged parts of the brain that cause Parkinson’s disease.
Parkinson’s disease develops when the brain cells (or neurons) that produce the chemical dopamine die or are damaged. Dopamine neurons produce a lubricant that helps the brain transmit signals to the body that control muscles and movement. When these cells die or are damaged the result is the shaking and muscle stiffness that are among the common symptoms of the disease.
"We are looking at a way of helping the brain to regenerate the dead or damaged cells that transport dopamine throughout the body," Dr Williams said. "Peptides help the body heal itself, providing many positive benefits for health, particularly in regenerative medicine; this is why the sports people were using them to recover more quickly in the current doping scandal."
Peptides are both the building blocks and the messengers of the body; the team has used them to mimic the normal brain environment and provide the chemical signals needed to help the brain function.
"Peptides stick together like Lego blocks, so in the first stage of the project we have been able to make a three dimensional material or tissue scaffold that provides the networks cells need to grow; but the peptides also carry instructions in the form of chemical signals which tell the cells to grow into new neurons," Dr Williams explained.
"Importantly, this material has the same consistency as the brain, does not cause chronic inflammation and is non-toxic to the body.
"Our aim is to use this scaffold material to support the patient’s own stem cells that could be turned into dopamine neurons and implanted back into the brain. We expect that when implanted the material and stem cells would be accepted by the brain as normal tissue and grow to replace the damaged or dead cells."
While the research is not yet complete, Dr Williams is excited by the possibilities this work offers to the treatment of degenerative conditions.
"It is no secret that we are living longer, and with this we are seeing an increase in many conditions that come about because of ageing such Parkinson’s. By developing biomaterials, like the ones we are working on, it could be possible to help the body to regenerate and provide an improved quality of life to the older members of our community," he said.
"This work can also be adapted to other parts of the body which struggle to repair themselves, such as new cartilage for joints, muscle and heart cells, bones and teeth. Ultimately, it will be like taking your car to the garage to have new parts fitted to replace the worn out ones."
The results of the first stage of this Australian Research Council funded project will be published in the international journal Soft Matter.
Discovery opens the door to a potential ‘molecular fountain of youth’
A new study led by researchers at the University of California, Berkeley, represents a major advance in the understanding of the molecular mechanisms behind aging while providing new hope for the development of targeted treatments for age-related degenerative diseases.
Researchers were able to turn back the molecular clock by infusing the blood stem cells of old mice with a longevity gene and rejuvenating the aged stem cells’ regenerative potential. The findings were published online in the journal Cell Reports.
The biologists found that SIRT3, one among a class of proteins known as sirtuins, plays an important role in helping aged blood stem cells cope with stress. When they infused the blood stem cells of old mice with SIRT3, the treatment boosted the formation of new blood cells, evidence of a reversal in the age-related decline in the old stem cells’ function.
“We already know that sirtuins regulate aging, but our study is really the first one demonstrating that sirtuins can reverse aging-associated degeneration, and I think that’s very exciting,” said study principal investigator Danica Chen, UC Berkeley assistant professor of nutritional science and toxicology. “This opens the door to potential treatments for age-related degenerative diseases.”
New research model to aid search for degenerative disease cures
Efforts to treat disorders like Lou Gehrig’s disease, Paget’s disease, inclusion body myopathy and dementiawill receive a considerable boost from a new research model created by UC Irvine scientists.
The team, led by pediatrician Dr. Virginia Kimonis, has developed a genetically modified mouse that exhibits many of the clinical features of human diseases largely triggered by mutations in the valosin-containing protein.
The mouse model will let researchers study how these now-incurable, degenerative disorders progress in vivo and will provide a platform for translational studies that could lead to lifesaving treatments.
“Currently, there are no effective therapies for VCP-associated diseases and related neurodegenerative disorders,” said Kimonis, a professor of pediatrics who specializes in genetics and metabolism. “This model will significantly spark new approaches to research directed toward the creation of novel treatment strategies.”
She and her team reported their discovery Sept. 28 online in PLOS ONE, a peer-reviewed, open-access journal.
The UCI researchers – from pediatrics, neurology, pathology and radiological sciences – specifically bred the first-ever “knock-in” mouse in which the normal VCP gene was substituted with one containing the common R155H mutation seen in humans with VCP-linked diseases. Subsequently, these mice exhibited the same muscle, brain and spinal cord pathology and bone abnormalities as these patients.
VCP is part of a system that maintains cell health by breaking down and clearing away old and damaged proteins that are no longer necessary. Mutations in the VCP gene disrupt the demolition process, and, as a result, excess and abnormal proteins may build up in muscle, bone and brain cells. These proteins form clumps that interfere with the cells’ normal functions and can lead to a range of disorders.
Another study carried out by members of this group – and published in August in the journal Cell Death & Disease – made use of these genetically altered mice to examine the development of Lou Gehrig’s disease, or ALS. The researchers, led by Dr. Hong Yin and Dr. John Weiss in UCI’s Department of Neurology, documented slow, extensive pathological changes in the spinal cord remarkably similar to changes observed in other animal models of ALS as well as in human patients. ALS research is currently limited by a paucity of animal models in which disease processes can be studied.
Genetically modified mice have become important research models in the effort to cure human ailments. Mice bred to exhibit the brain pathology of Alzheimer’s disease, for example, have dramatically sped up the race to advance new treatments – one such model was developed at UCI. And many cancer therapies were created and tested using genetically altered mice.
(Source: today.uci.edu)
Researchers identify mechanisms that allow embryonic stem cells to become any cell in the human body
July 18, 2012
(Phys.org) — New research at the Hebrew University of Jerusalem sheds light on pluripotency—the ability of embryonic stem cells to renew themselves indefinitely and to differentiate into all types of mature cells. Solving this problem, which is a major challenge in modern biology, could expedite the use of embryonic stem cells in cell therapy and regenerative medicine. If scientists can replicate the mechanisms that make pluripotency possible, they could create cells in the laboratory which could be implanted in humans to cure diseases characterized by cell death, such as Alzheimer’s, Parkinson’s, diabetes and other degenerative diseases.
To shed light on these processes, researchers in the lab of Dr. Eran Meshorer, in the Department of Genetics at the Hebrew University’s Alexander Silberman Institute of Life Sciences, are combining molecular, microscopic and genomic approaches. Meshorer’s team is focusing on epigenetic pathways—which cause biological changes without a corresponding change in the DNA sequence—that are specific to embryonic stem cells.
The molecular basis for epigenetic mechanisms is chromatin, which is comprised of a cell’s DNA and structural and regulatory proteins. In groundbreaking research performed by Shai Melcer, a PhD student in the Meshorer lab, the mechanisms which support an “open” chromatin conformation in embryonic stem cells were examined. The researchers found that chromatin is less condensed in embryonic stem cells, allowing them the flexibility or “functional plasticity” to turn into any kind of cell.
A distinct pattern of chemical modifications of chromatin structural proteins (referred to as the acetylation and methylation of histones) enables a looser chromatin configuration in embryonic stem cells. During the early stages of differentiation, this pattern changes to facilitate chromatin compaction.
But even more interestingly, the authors found that a nuclear lamina protein, lamin A, is also a part of the secret. In all differentiated cell types, lamin A binds compacted domains of chromatin and anchors them to the cell’s nuclear envelope. Lamin A is absent from embryonic stem cells and this may enable the freer, more dynamic chromatin state in the cell nucleus. The authors believe that chromatin plasticity is tantamount to functional plasticity since chromatin is made up of DNA that includes all genes and codes for all proteins in any living cell. Understanding the mechanisms that regulate chromatin function will enable intelligent manipulations of embryonic stem cells in the future.
"If we can apply this new understanding about the mechanisms that give embryonic stem cells their plasticity, then we can increase or decrease the dynamics of the proteins that bind DNA and thereby increase or decrease the cells’ differentiation potential," concludes Dr. Meshorer. “This could expedite the use of embryonic stem cells in cell therapy and regenerative medicine, by enabling the creation of cells in the laboratory which could be implanted in humans to cure diseases characterized by cell death, such as Alzheimer’s, Parkinson’s, diabetes and other degenerative diseases.”
Source: PHYS.ORG