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Tag Archives: Huntington’s

Friday Science Review: February 5, 2010

Several neurological related stories this week and quantum biology?

Glial Cells – They’ll turn against you: An unusual molecule can turn glial cells, which normally surround neurons, into killer cells that attack the neurons they are suppose to protect.  Researchers made the surprising discovery of proNGF’s role while trying to figure out its function in the eye.  They found that it can activate glial cells to turn against retinal neurons and potentially cause vision impairment or loss.  Some of the molecular details were also worked out and they describe the significance of TNFalpha and p75NTR proteins in this cell death process.  These results shed light on potential routes for therapeutic targets to prevent certain cases of vision loss.  The study, published in the early on-line edition of the Proceedings of the National Academy of Sciences, is a collaboration involving Dr. Adriana Di Polo at Université de Montreal and Dr. Philip Barker at the Montreal Neurological Institute.

Unexpected Heart Failure and Treatment: Researchers studying mouse models for neuronal diseases, such as Alzheimer’s, noticed progressive abnormalities in the rodent’s heart function.  The mice had slower heart rates (as expected) but they also had difficulty pumping blood and researchers soon realized that they may have stumbled upon a possible mechanism of human heart failure.  The genetic modification in these mice resulted in decreased levels of the neurotransmitter, acetylcholine.  In contrast to previous reports on heart failure, this is the first study suggesting that slower heart rates may lead to cardiac dysfunction.  Furthermore, the administration of the drug Pyridostigmine, which increases acetylcholine levels and is approved for treating muscle weakness, corrected the cardiac dysfunction.  The research team of Drs. Marco Prado and Vania Prado at the Robarts Research Institute at The University of Western Ontario describe their findings in the latest edition of Molecular and Cellular Biology.

Early Stages of Huntington’s: Insight into the cellular mechanisms in the brain that causes Huntington’s disease is described in this article appearing in the journal Neuron.  Using mouse models expressing the gene mutations causing the disease, scientists discovered increased numbers of NMDA receptors surrounding the synaptic connections between neurons.  The increased NMDA receptor activity also diminishes survival signals leading to brain cell death.  In other words, the neurons become confused and triggers cell death (excitotoxicity).  Although it is not known why the receptors accumulate outside of the neuron, a therapeutic drug is already available (for Alzheimer’s) to treat the early stages of the disease.  Memantine can control the abnormal NMDA receptor signaling specifically outside the synapses and not disrupt the normal activity within the synapse, thereby reducing side effects.  Clinical trials are underway.  Dr. Lynn Raymond at the University of British Columbia led the research team.

Algae + Quantum Biology?: It appears that algae, a very simple organism, figured out quantum mechanics nearly two billion years ago.  During the process of photosynthesis, antenna proteins in the light-harvesting complexes absorb light and transmit the energy between molecules to proteins in the reaction centre.  Researchers at the University of Toronto decided to study this energy transfer and discovered quantum mechanics at play in this photosynthetic process.  This is just a bit beyond the scope of our blog but you can read Drs. Greg Scholes and Paul Brumer’s commentary here or enrich yourself with the detailed study here in the journal Nature.

Friday Science Review: July 31, 2009

My first post… a two week round-up.

New direction for treating obesity:  A study headed by Dr. Hans-Michael Dosch’s group at The Hostpital for Sick Children in Toronto demonstrated that killer T cells in visceral fat are activated to destroy fat cells and control insulin resistance.  With increasing weight gain, however, the killer T cells become overwhelmed as fat cells grow and inflammatory T cells move in.  Although these studies were performed in mice, it appears that humans also have a similar system in place.  The good news is that treatment with an anti-CD3 drug can give the immune system a boost and help reduce inflammatory T cells.  Even better news is that this drug is already in clinical use to protect against organ rejection, which means clinical trials to combat obesity may start as early as next year.  The article was published on-line this week in Nature Medicine.

Cool headed Toucan.  After decades of speculation over the purpose of the toucan’s over-sized beak – from sexual ornament to feeding purposes – researchers at Brock University in Ontario, in collaboration with scientists in Brazil, published an article in Science showing that the toucan’s beak acts as a highly efficient cooling unit.  They have the greatest beak-to-body size ratio and use this large surface area as a heat exchanger (akin to elephants’ ears) to regulate body temperature by modifying blood flow.  If only we had a ‘heat wave’ problem this summer…

Setback in Huntington’s Disease research.  A decade long study concluding with disappointing results was reported in PNAS this week.  Researchers at Laval University and University of South Florida analyzed the brains of HD patients who had undergone neural transplantations about ten years ago as a potential treatment.  Although there were mild clinical benefits, the grafts were short-lived and also had undergone disease-like degeneration.

Barcoding Nemo. As part of the International Barcode of Life Project to identify all plants and animals based on signature DNA sequences, spear-headed by Paul Herbert at the University of Guelph, the ornamental fish was added to the list.  Accurate identification of ornamental fish is important for establishing regulations, conservation practices and tracking origins.  The DNA barcode reference for these fish is based on the cytochrome c oxidase subunit I (COI) gene where 98% of the fish have distinct barcode clusters.  The article was published in PLoS One last week.

Funny etiology: two curious New York high schoolers initiated the project and recruited the Guelph lab, sparking headlines last summer when they discovered that some sushi restaurants were mislabeling cheaper fish as more expensive types.

Other DNA barcoding projects include other fish, butterflies, and birds.  To find out more, visit the Canadian Centre for DNA Barcoding or the International Barcode of Life Project (iBOL).

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