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How the Brain Falls Prey to Alzheimer’s Disease

7/15/2012

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First-ever timeline details the evolution of Alzheimer's disease over the years
Scientists with the Dominantly Inherited Alzheimer’s Network (DIAN) international research partnership say that they were recently able to develop the first clear timeline detailing how the brain develops Alzheimer’s disease. 

The new dataset will come in handy for researchers who are working hard towards finding ways of addressing the condition. Alzheimer’s is a neurodegenerative form of dementia that currently has no cure. Its primary mode of action is by damaging neurons and attacking cognitive capabilities. 

Since it primarily manifests itself in the elderly, and the general population of the developed world is growing, the condition is expected to put huge strains on national healthcare systems over the coming decades, PsychCentral reports. 


While the therapies experts managed to propose thus far have largely proven ineffectively at treating the condition, some have argued that this is because the dementia starts manifesting clear symptoms only after it has already taken a hold of the brain.

But the team behind the new dataset, which also included scientists from the University of Washington in St. Louis (WUSL) School of Medicine (WUSM), suggests that the earliest signs of the condition set in as many as 25 years before the first discernible symptoms appear. 

In order to compare the new timeline, the investigators looked at a series of markers for Alzheimer’s disease that appear long before the condition sets in. This was made possible by surveying 128 test subjects who came from families whose genetic history predisposed them to developing the disease.

“A series of changes begins in the brain decades before the symptoms of Alzheimer’s disease are noticed by patients or families, and this cascade of events may provide a timeline for symptomatic onset,” WUSM expert and lead study author, Randall Bateman, MD, says.

“Family members without the Alzheimer’s mutations have no detected change in the markers we tested. It’s striking how normal the Alzheimer’s markers are in family members without a mutation,” he goes on to say. 

The research was made possible by funds provided through the US National Institutes of Health (NIH). Details of the work were published in the latest issue of the prestigious New England Journal of Medicine.

“As we learn more about the origins of Alzheimer’s to plan preventive treatments, this Alzheimer’s timeline will be invaluable for successful drug trials,” Bateman concludes.


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New Cell Delivery Technologies in the Works

7/15/2012

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This image shows microbeads developed by SpherIngenics for cell delivery within the human body
A startup from the Georgia Institute of Technology (Georgia Tech) has recently secured funding from the US Department of Defense (DOD), for the development of new technologies related to delivering cells to any location within the human body. 

Cell delivery is a critical step in the process of repairing damaged tissues. However, the main issue with putting new cells in the body is that the environment they encounter once they reach the bloodstream is extremely hostile. 

Any new structures inserted into the body are immediately attacked and disintegrated by the immune system. This leads to significant inflammation, a condition that poses its own set of problems. If the therapeutic cells are not destroyed by this response, they are at least scattered in all directions.


This means that the impact they were supposed to have on a particular area will be severely diminished. In most cases, the cell injections end up having no effect, but producing multiple side-effects. The new startup, called SpherIngenics, was created as a method of preventing this from happening. 

In order to do this, the company is using technology developed in the Wallace H. Coulter Department of Biomedical Engineering at Georgia Tech, and at the Emory University. Their method is safe, reliable, yields no significant side-effects, and is entirely repeatable.

In addition to protecting the newly introduced cells from an untimely death, they also prevent them from migrating to other locations in the body, increasing the efficiency of cell delivery therapies by a wide margin. SpherIngenics hopes to capitalize on this approach by creating new protective capsules.

Its efforts are being supported by a two-year, $730,000 Phase II Small Business Innovation Research (SBIR) grant from the DOD. The company was funded by Coulter Department professors Franklin Bost (also the company's CEO), Barbara Boyan and Zvi Schwartz.

“When damaged tissue is being repaired by a cell-based therapy, our microbead technology ensures that cells travel to and remain in the targeted area while maintaining continued viability,” Bost explains.

“This technology has the potential to reduce the cost of treatment by eliminating the need for multiple therapeutic procedures,” the expert goes on to say. SphereIngenics was founded back in 2007.

“For the Phase II SBIR grant, we’re going to examine whether delivering microbeads full of stem cells can enhance cartilage repair and regeneration of craniofacial defects in an animal model,” Boyan adds.


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Gene loss causes leukemia

6/1/2010

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The PTPN2 gene plays an important role in hindering the development of T-ALL leukemia
                                                   Researchers from VIB and K.U.Leuven, both in Flanders, Belgium, have discovered a new factor in the development of acute lymphoblastic leukemia, a disease that mainly affects children. In the cells of the patients, the specific  gene PTPN2 ceases to function, causing the cancer cells to survive longer and grow  faster. The study provides genetic and functional evidence for a tumor suppressor role of  PTPN2. The research was carried out in close cooperation with scientists from the Hôpital  Saint-Louis in Paris. Understanding the causes of leukemia is important for the development of new targeted therapies. The results appear in the journal Nature Genetics.

 

What is leukemia or bone cancer?

In patients with leukemia, the formation of white blood cells in the bone marrow is disrupted. This
makes leukemia patients particularly susceptible to infections, because properly functioning white
blood cells ensure protection against intruders such as viruses and bacteria. In the US alone, every
year around 50.000 adults and children develop leukemia.

 

T-ALL is caused by interplay of various factors

Leukemia occurs in various forms, one of which is T-cell acute lymphoblastic leukemia (T-ALL). Cells
that normally develop into white blood cells, start to divide in an uncontrolled way, giving rise to a
huge number of immature cells. Until now, few factors have been associated with an increased risk of
developing T-ALL, but it is clear that T-ALL develops when errors occur in several genes
simultaneously. Therefore, it is not only important to identify genes that underlie T-ALL, but also to
unravel what combinations give rise to the disease. This is a crucial element in the development of
future specific combination therapies, promising to be more effective than therapies that focus only on
one target.

 

PTPN2 has a tumor suppressor role

Maria Kleppe and Jan Cools of VIB-K.U.Leuven, together with Peter Vandenberghe of the Centre for
Human Genetics and Jean Soulier of the Hôpital Saint-Louis in Paris, now identified the gene PTPN2 as
another major player. In the DNA of the cells of some leukemia patients, they noticed that the PTPN2
gene was lost, causing proliferation of the cancerous cells. In addition, PTPN2 was identified as a
negative regulator of the activity of a specific kinase. The study provides genetic and functional
evidence for a tumor suppressor role of PTPN2.

 

Kinases and phosphatases in cancer development

Beyond the specific findings for T-ALL, this study provides new insights into cancer development in
general. Errors in kinases and phosphatases, enzymes able to switch specific cellular functions on of
and off, have long been known as potential causes of cancer, but this study now shows that when
these errors occur together, the carcinogenic effects can reinforce each other. Furthermore, they can
make the cells more resistant to kinase inhibitors, therapeutic substances currently used for cancer
treatment.
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