Greenberg also possesses the mental capacity of an infant, and has never learned to speak or eat on her own. According to a recent report on ABC:

Brooke hasn't aged in the conventional sense. Dr. Richard Walker of the University of South Florida College of Medicine, in Tampa, says Brooke's body is not developing as a coordinated unit, but as independent parts that are out of sync. She has never been diagnosed with any known genetic syndrome or chromosomal abnormality that would help explain why.

She has also suffered from several strange maladies, including burst ulcers, a stroke and a brain tumor, which healed after Greenberg appeared on the verge of death.

It's unclear whether her capacity to heal is related to her agelessness, but researchers hope to find out. ABC reports:

Geneticist Maxine Sutcliffe chronicled a baffling range of inconsistencies in Brooke's aging process. She still has baby teeth at 16, for instance. And her bone age is estimated to be more like 10 years old.

"There've been very minimal changes in Brooke's brain," Walker said. "Various parts of her body, rather than all being at the same stage, seem to be disconnected."

Greenberg sleeps in a crib, and attends school. Her teachers and family aren't sure how much she understands, but they say she recognizes people familiar to her and likes to play and laugh.

Currently geneticists are trying to isolate the gene or set of genes responsible for her bizarre aging process. There are no other known cases like Greenberg's, and it's possible that her genome could be the key to unlocking how our bodies know when to age. If a sixteen-year-old can look like a sixteen-month-old, then why couldn't a sixty-year-old look twenty-one? Of course, treatments based on Greenberg's condition might keep people's brains stuck at the same age as their bodies. So you wouldn't have a person with the wisdom of a sixty-year-old in a youthful package. You'd just have somebody whose mind remained twenty-one for decades on end. Which sounds cool until you really think about it.

via ABC

Here is how the authors of the study describe what you're seeing in these images:

(A) Wild type (negative control). Wild type primary neurons in a mature culture show cell body clusters interconnected by well-fasciculated axon tracts. (B) Int6 transcription initiation factor knockdowns show extensive defasciculation. (C) Ran GTPase RNAi cultures have both excessive branching and defasciculation. (D) Huntingtin knockdowns show a moderate level of excessive branching. (E) Sec61α RNAi shows poor connectivity between cell clusters and highly branched, defasciculated neurons. (F) Diablo (cytoskeletal binding protein). Diablo knockdown leads to a primarily defasciculated phenotype. (G) CG12082 (novel gene) RNAi causes reduced connectivity between cell clusters, excessive branching and defasciculation. (H) Lpr2 LDL receptor knockdowns show excessive branching and defasciculation, yet with robust outgrowth. (I) Dopamine 2-like Receptor RNAi shows defasciculation.

A translation, as far as I am able to provide it, is that image (A) is an untreated bunch of neurons called a "wild type" (this is a term used for any non-modified or genetically engineered organism). The rest of the images are of neurons whose structure has been changed by the RNAi process. Don't worry — these are all fruitfly neurons. No human brains were harmed in the making of these cool images. Images via PLoS Genetics.

All four families have a few things in common. First, the people with Unertan syndrome are all the products of incestuous marriages. Children of closely-related people often suffer birth defects. Also, the children who walk on all fours are developmentally disabled; some are unable to talk. What shocked the researchers was that the families with quadrupedal members did not share the same kinds of genetic mutations. One of the researchers, Tayfun Ozcelik, gave a talk today at the European Society of Human Genetics about the genetic study. According to a release from the Society:

Although the families lived in isolated villages 200-300 km apart and reported no ancestral relationships, the scientists expected to find a single genetic mutation implicated in the condition. They were surprised to find that this was not the case.

"We carried out genome-wide screening on these families", said Professor Ozcelik, "and found regions of DNA that were shared by all those family members who walk on all fours. However, we were surprised to find that genes on three different chromosomes are responsible for the condition in four different families.

"In families A and D there were mutations in VLDLR on chromosome 9, and in family B the phenotype maps to chromosome 17 to a region that contains at least 157 genes, and we are still looking for the precise mutation. Neither region appears to be implicated for family C."

In all cases, the affected individuals were the offspring of consanguineous marriages, which suggests that if they had married outside the family they would not have had the condition. All of them had significant developmental delay in infancy. "Whereas normal infants make the transition to walking on two legs in a relatively short period", said Professor Ozcelik, "these individuals continued to move on their palms and feet and never walked upright. Although they can stand from a sitting position and maintain this upright position with flexed hips and knees, they virtually never initiate bipedal walking on their own."

It has been suggested in the past that lack of access to medical care exacerbated the effects of an under-developed cerebellum, and that this led to quadrupedality. "Although it may be true that family B lacked proper medical care, families A and D had consistent access to good medical attention, and both families sought a correction of quadrupedality in their affected children", said Professor Ozcelik. "Indeed, an unaffected member of family A is a physician, who has been actively involved in the medical interventions. In addition, the parents in family A also discouraged their affected children from walking on all fours, to no avail. We think that social factors are unlikely to be involved in the development of quadrupedal locomotion."

Along with brain enlargement, speech, and the ability to make tools, upright walking has long been regarded as one of the key traits that have led to modern humans. Professor Ozcelik's team have opened a window on how mutations in VLDLR affect brain development and influence gait in humans.

"It will be interesting to see if the VLDLR gene is involved in other types of cerebellar ataxias. In addition, we hope to identify the defective genes associated with quadrupedal locomotion in families B and C", he says.

All the families do share genetic factors in common, and Ozcelik's team says similar genetic factors are found in a few North American families whose members cannot walk at all.

If it turns out that there are several groups of genes that control for bipedalism, it might be possible to genetically modify people to walk on all fours. It's hard to imagine why anyone would want to do this outside a mad scientist movie. However, many human genes are shared with our quadrupedal mammalian cousins. Perhaps discovery of the bipedal gene could be the first step in helping cats, dogs, and apes to walk upright. Yes, it could be the first key to "uplifting" other species.

Genetic Mutation Linked to Walking on All Fours [Eurekalert]

According to the study that revealed these dire statistics, a HEPA filter could stop many of the mutations from happening. A release about the study says:

Mice breathing unfiltered, polluted air downwind of a large industrial area [near two steel mills and a major highway in Ontario, Canada] developed 60 percent more mutations in their sperm than mice whose air was cleaned with HEPA filters . . . The report expands on previous research and suggests that the mutations are not due to the animals' mixed genetic background.

AP Photo/Color China Photo

Germ-line mutations, DNA damage, and global hypermethylation in mice exposed to particulate air pollution in an urban/industrial location [PNAS]

This all started with a remake of John Carpenter's The Fog back in 2005, and these foggy mutant films just keep rolling in. Based on the box office numbers from the Fog remake and The Mist (it's just about to drop out of the top ten, where it debuted at #8), it's unclear why Hollywood is so into this trend.

The good news is that comic book publisher Studio 407, publishers of Night & Fog, signed a first-look deal with Myriad Pictures, and that means its indie properties will begin the arduous Hollywood development cycle very soon. While it's nice to see deals with companies other than Marvel and DC, we hope there will be a few original storylines tossed into the mix.

Myriad, 407 On Drawing Board [Hollywood Reporter]