This is the surprising news from a team of researchers are the University of Szeged, Hungary. The researchers made the discovery by analyzing a type of neuron called neurogliaforms. Neurogliaform cells (also called dwarf cells or dwarf neurons) are GABAergic neurons – they release the GABA neurotransmitter (the primary inhibitor in the central nervous system).

Neurogliaform cells are widely distributed in the cortex and are involved in many cognitive functions including attention, language, learning, memory, and perception. All of this was known before the team, led by Gábor Tamás, began their study. What was not fully understood was how neurogliaforms communicate.

The group used electron microscopes to analyze brain tissue, which showed that neurogliaform cells have bushy axons with many branches. They examined the terminals at the end of these axons (axonal boutons) and found that of the 50 boutons studied, only 11 formed synapses. In other words, the majority (approximately 78%) of do not form “classical” synapses. My old neuroscience lecturer would have had a fit! If they are not forming synapses, then how are they communicating?

It would appear that the cells are communicating using a mechanism called volume transmission, where the GABA is diffusing in a cloud through the extracellular fluid. The bushy structure of these neurons would seem to be ideal for this type of signaling. Subsequent experiments by the group confirmed that a single neurogliaform can release enough GABA to inhibit nearby neurons, even when no synapses are present.

Another set of experiments showed that neurogliaforms contain receptors that can detect very low levels of GABA. This suggests that they are purpose-built to communicate among themselves, again in the absence of synapses.

This is truly groundbreaking stuff. Just as Francis Crick’s central dogma of molecular biology has gradually yielded to some unexpected molecular acrobatics, so too the dogma of synaptic neurotransmission must be rewritten. Certainly, synapses will remain the main players, but now there is a little competition on the pitch.

A student then asked what happens to someone if they get a blood transfusion. He was concerned since receiving blood from another person would mean you had the cells of the other person inside of you. He said, “Would that change the way you look?” The student seemed worried by the idea that the cells in the new blood would contain the DNA of another person. Since cells use the information in the DNA to determine our traits, he assumed that there was the possibility that a blood transfusion could change the way that you look.

While receiving a blood transfusion will not change your hair or eyes, the new cells you get will help you survive if you have lost too much of your own blood. The new blood contains the plasma (liquid), red blood cells, white blood cells, and platelets. The blood fills up the volume of what you have lost while the new cells can perform a variety of functions, including the transport of oxygen. Even though the new cells do have new DNA, the cells will only be using the recipes to help them work as blood cells. In addition, these cells will die and be replaced by your own new blood cells with your own DNA.

Affectionately known as “Ardi”, some of her features were distinctive. Due to her location in the ancient Ethiopian strata, she was dated to 4.4 million years ago, pre-dating “Lucy” (Australopithecus afarensis) by over a million years. Her brain size was much smaller than Lucy’s but was similar to that of a modern chimpanzee.  According to the form of her limbs and pelvis, she was able to walk upright, yet she had a grasping hallux (big toe) on each foot, which suggests that she had an arboreal lifestyle.  This theory was supported by the fossils discovered locally near Ardi’s resting place.  This “woodland” lifestyle came as a surprise to scientists because Ardi’s descendant, Australopithecus afarensis (”Lucy”), lived on the savannah.  Now thoughts on the evolution of bipedalism must be re-threaded.  

To date, Ardi (Ardipithecus ramidus) has replaced Lucy (Australopithecus afarensis) as the oldest hominid fossil.  Genetically, the common ancestor between humans and chimps was estimated to exist 6 million years ago.  “Ardi” takes us one step closer to that ancestor.

For more on Ardi, see our interview with researcher, Tim White, at the DNALC website here.  

Ardi sketch redirected from The Guardian.

Any individual has a unique genetic profile different from that of another person. Contained within these differences are unique genetic variations that may make a person more susceptible to diseases such as cancer and diabetes. There are genetic profiling centers that can assist you in identifying your genetic variations. With this information you and your physician can watch your health where it is at risk to becoming a problem and mold a life style toward prolonged health. In order to decrease the impact of a possible problem, it is important that you’re analysis be broad-spectrum and precise. It will be of great interest to identify the premier centers for analysis of genetic variants. Be curious and talk with your physician about the resources that will give you the edge in enhancing your quality of life.

The most mystifying of the model organisms is the plant.  How could a scientist possibly learn anything about human genetics from a plant?  One popular model from the plant kingdom is a weed from the mustard family found all around the world called Arabidopsis, or Thale Cress. It has a small genome, and as such, was the first fully sequenced plant genome!  In addition to studying plant traits useful for agriculture, such as light sensitivity and flowering, there are other important cellular traits being studied in plants.

What most students don’t realize (until they are actually asked to think about it) is that all cells perform basic functions, and these basic functions are required for life. Interestingly enough, mutations in genes involved in the regulation of the most basic cell functions such as cell division, are the culprits in diseases such as cancer.  Telomeres, structures that cap chromosomes, are found in plant and animal cells and also play a potential role in basic functions like cell division.  Recent Arabidopsis research may shed light on the relationship between telomeres and cancer!

So the next time you’re out weeding the garden, take a moment to consider this: that plant you’re uprooting may contain valuable information!

According to research published in the Journal, Cerebral Cortex, by Stephanie McHughen  et.al., a key SNP in BDNF (valine 66 mutated to methionine) impacts learning and memory functions, cognitive tools which happen to be crucial for operating an automobile.

During one of the described experiments, subjects were seated at a computer, with attached steering wheel as they had to keep the virtual car on a black line in the center of the screen. Subjects got to learn the driving circuit by following the car on 15, 60 second trials.  While both groups of subjects (those who had the “normal” valine  allele, and those with the val⁶⁶met SNP) started at similar levels of ability, and showed short term learning. During the trials however, val⁶⁶met subjects showed less learning, and made more mistakes while learning. By day 5 of training, those with the val⁶⁶met allele showed less ability to retain the skills they had learned. The study also showed some differences in the activation of regions of the brain responsible for motor function and learning, such as the motor cortex.

Having this SNP is not all bad, as the val⁶⁶met SNP appears to be advantageous in disease settings, such as Alzheimer’s, Parkinson’s or multiple sclerosis, as it is thought that this SNP can increase the stability of certain brain functions, even though they may reduce plasticity in some learning tasks. In other words, this polymorphism may be the middle ground between flexibility and durability in brain functions.

I actually didn’t pass my road tests the first few times, and since my genotype happens to be heterozygous for this SNP I now have an excuse! My cello playing was never yo-yo ma, and but my teacher always commented that I had such a better time with difficult passages than simple ones. I wonder how this affects fine motor skills?

Jason – rs6265 (A/G)

The nucleus, where chromosomal DNA is stored and protected, is not the only source of DNA in a mammalian cell.  Mitochondria have their own 16,569 bp genomes encoding 37 genes involved in the production of biological energy, ATP.  Mutations in these genes have been linked with human diseases including diabetes, cancer, infertility, and neurodegeneration.  Women who carry a mixture of normal and mutated mitochondrial DNA, a condition called heteroplasmy, may be physiologically healthy but risk having seriously ill children.  The birth of Mito and Tracker, at the Oregon Health and Science University (OHSU), suggests that there may be a way for heteroplasmic women to bear healthy, (mostly) biological children.

When one female’s chromosomal DNA is transferred into another’s enucleated egg cell, the first female’s mitochondrial genome is replaced.  The resulting child features mom’s and dad’s chromosomal DNA, but also carries a donor female’s mitochondrial DNA.  Should the DNA transfer technique work in human cells, “who’s my other mommy” could be a question for the courts.

The underlying cause for FXTAS is a mutation in the gene for Fragile X Mental Retardation Protein (FMRP), which is located on the X-chromosome; its protein product, Pur-α is essential for normal neural function. Scientists have recently determined the three-dimensional structure for this protein, a first step in the potential identification of an effective treatment that would address the cause and not just the symptoms of FXTAS.

As described in Your Genes, Your Health, the gene contains a region that consists of repeated CGG DNA triplets. In healthy people, both copies of their FMRP gene contain 5-54 copies of the CGG triplet. Disorder manifests itself if the repeat numbers exceed 54 in both gene copies (the disorder is recessive): 55-200 repeats lead to FXTAS, as described above. Repeat numbers exceeding 200 lead to Fragile X Syndrome (FXS), the second most common cause of heritable mental impairment after Down’s syndrome.

Given that the symptoms of FXTAS include shaking hands, it is interesting that the authors describe the shape of the FMRP protein, Pur-α as: “The crystal structure of Pur-α … looks like a hand: four so-called beta-strands, corresponding to four fingers, form a beta-sheet, and an adjacent alpha-helix resembles a thumb.” Apparently, pairs of PUR repeats bind to each other in a configuration that is reminiscent of a handshake, forming a functional unit that binds to RNA.

These definitions stress differences that occupied either end of a continuum of eugenics practice. At one end, Galton’s definition stressed social control, or laws, to control human reproduction. At the other end, Charles Davenport’s stressed an individual’s own control over their reproduction. Social control ultimately embodied “negative eugenics”– limiting mixed race marriages, restricting immigration from southern and eastern Europe, and sterilizing mental and epileptic patients. Self-direction embodied “positive eugenics” – taking personal measures to improve one’s own genetic heritage through mate selection.

Of course, things weren’t that simple. Galton never strongly advocated for negative eugenics, and England never inacted coercive eugenics legislation. To the contrary, Davenport’s Eugenics Record Office successfully lobbied state governments and the U.S. congress to enact restrictive eugenics legislation that culminated in the U.S. Supreme Court upholding the premise of compulsory sterilization.

The Holocaust represented the nadir of eugenic practice, but it would be wrong to think eugenics ended with the Nazis. As examples, ethnic cleansings continue to this day in Darfur, and disincentives against large families trump personal reproductive wishes in China. At the same time, fertility drugs and in vitro fertilization extend reproduction to infertile couples, and pre-implantation DNA diagnosis puts the ultimate slant on the notion of self-directing of human evolution.

And somewhere in between is the simple act of picking the healthiest, most virile mate we can find to help us propel our genes into the future. We all lie somewhere on the continuum of eugenics practice.

You may not know this, but dogs can actually smell some cancers. It doesn’t even take a sophisticated sniffer dog to do this: even some household dogs can be trained to tell the difference between the odor of a normal person and that of a person with lung cancer. In theory, your dog Max could be a living cancer detector, letting you know early on that you are at risk.

Dogs also get cancers. If fact, cancer is the number one killer of dogs, and about one in three dogs get cancer. Every year, almost a million dogs die of cancer in the United States. Often, cancers in dogs are treated with the same treatments that are used in humans. This is because dogs and people are very similar, so many of the drugs developed to treat people work on dogs. This summer, the first cancer drug specifically for dogs was approved by the FDA. The drug, called Palladia, shrinks the size of mast cell tumors by killing tumor cells and cutting off their blood supply. If you are a dog owner, this may be reassuring: at least one drug has now been tested on dogs before it goes into use.

Dogs and their owners are now being called into service in a different way. In an effort to speed up testing of promising drugs, some experimental cancer drugs are being offered to owners with afflicted canines.

Of course, some people will think that using pets as “guinea pigs” in experiments (sorry guinea pig lovers…) is unethical. Even though researchers will make the well-being of the dogs a priority, it is difficult to predict the outcome of these experiments. With luck, the dogs will benefit and the new drugs will be made available to people sooner than they would be otherwise. For those unlucky dogs that don’t benefit, my thanks, much as I thank the brave people who take experimental drugs.