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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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Megavirus May Be Stripped-Down Version of Normal Cell

10/15/2011

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About five years ago, biologists were surprised by the first discovery of an extremely large virus. Viruses are generally stripped down, efficient predators, only carrying as much DNA or RNA necessary to hijack their host and make extra copies of themselves. The newly discovered virus, called Mimivirus, was anything but stripped down; it carried a genome nearly the size of some bacterial species. And, instead of simply hijacking its host, the viral genome carried a lot of genes that replaced basic cellular functions, including some involved in DNA repair and the manufacturing of proteins.

The unusual size and gene content of the virus led one scientist to suggest that viruses could explain the origin of DNA-based life. If viruses carried all these genes, then it’s possible to imagine that one could set up shop in a cell and simply never leave, gradually taking over the remaining functions once performed by its host’s genetic material. This would explain the origin of DNA, which would distinguish the virus from its host’s genetic material, a holdover fromthe RNA world. It could also explain the existence of a distinct nucleus within Eukaryotic cells.

A paper is being released today, however, that argues that this scenario has things exactly backwards. Giant viruses, its authors argue, have all these genes normally associated with cells because, in their distant evolutionary past, they were once cells.

Mimivirus was discovered in an amoeba, so the authors of the new paper used a simple technique to look for its relatives: take three different species of amoeba, expose them to a variety of environmental samples, and see if anything big starts growing in them. They hit pay dirt with a sample obtained from an ocean monitoring station just off the coast of Chile. Despite the oceanic source, the virus grew nicely in fresh water amoebae. The site also gave the virus its name: Megavirus chilensis.

The authors followed its lifestyle, showing that it behaved much like Mimivirus, forming similar structures within its host cell that could only be distinguished using electron microscopy. They also sequenced its entire genome, which turned out to be the largest virus genome yet completed: 1.26 million base pairs of DNA (Megabases). Based on this sequence, Megavirus is a distant cousin of Mimivirus. Of its 1,120 protein-coding genes, over 250 have no equivalent in Mimivirus. But, of the genes that are shared, the sequences average about 50 percent identity on the protein level. This means that Megavirus is similar enough that it can be compared to Mimivirus, but different enough that it’s possible to make some inferences about the viruses’ evolutionary history.

And what they find supports the view that the virus started out with a much larger complement of genes. For example, Mimivirus has a suite of genes that can help repair DNA. Megavirus has those plus one other that is specialized for the repair of DNA damaged by UV light. The additional gene appears to be functional: Megavirus was able to grow following an exposure to UV that was sufficient to disable Mimivirus.

Both viruses share an identical set of genes involved in transcribing their DNA into RNA, and use an identical set of signals to indicate where the transcripts should start and stop. Mimivirus also contains a number of genes used in the translation of RNA into protein. Megavirus has those plus a few more, including additional genes that attach amino acids (components of proteins) onto RNAs for use in translation.

Clearly, the common genes suggest that the viruses share a common ancestor. This leaves two possibilities for the novel ones: either the ancestral virus had a larger collection and its descendants have lost different ones, or each virus picked up different genes from its hosts through a process called horizontal gene transfer. The authors favor the former explanation, because most of the genes specific to one of the two viruses don’t look like any gene present in their hosts (or any other gene we’ve ever seen, for that matter). This implies that horizontal gene transfer doesn’t seem to have done much to shape the viruses’ genomes.

So, when did the common ancestor exist? The authors line up a few of the conserved megavirus genes (including those of a more distantly related giant virus, CroV) with the equivalents in other eukaryotic species, and find that they branch off right at the base of the the eukaryotic lineage. In other words, the viruses seem to have had a common ancestor with eukaryotes, but it split off right after the eukaryotes diverged from bacteria and archaea. (This also argues against the horizontal gene transfer idea, since there doesn’t seem to be a species out there that the genes could have been transferred from.)

To the authors, this suggests that the viruses are the evolutionary descendants of an ancient, free-living eukaryotic cell. Various genes and structures from that organism have gradually been lost over its long history as a parasite, leaving something that propagates like a virus, but belongs to a distinct lineage from all other viruses that we’re aware of.

The authors make a reasonably compelling case against the megaviruses getting their complex genomes via horizontal gene transfer, although it would be good to see a similar analysis for a lot more of the shared genes. What they don’t do, however, is rule out the initial alternative: it’s still technically possible that the megaviruses and eukaryotes share an ancient common ancestor because all eukaryotes are descendants of the virus’ genome. At the moment, I’m not sure it’s possible to distinguish between these alternative explanations.
Citation: “Distant Mimivirus relative with a larger genome highlights the fundamental features of Megaviridae.” By Defne Arslan, Matthieu Legendre, Virginie Seltzer, Chantal Abergel and Jean-Michel Claverie. PNAS, published online Oct. 10, 2011. DOI: 10.1073/pnas.1110889108

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