Prions

Zombies at the Molecular Level

We've seen the cheesy zombie films. Mindless living dead creatures with the only goal to harass the living, often with the intent to dine on their brains. Where the newly and unfortunately lobotomized victims soon after also become zombies with the same insatiable platelet. Soon after everyone in town is transformed.

As incredulous as this sounds, a story along these lines is a plausible threat and a cause for much concern. Although the gravity of the situation is great, the scale at which these mutants operate is minuscule. I refer to the "mutated" proteins known to as prions.

Prions arise from endogenous proteins (referred to as PrPc) found in brain tissue, its native function has not been fully elucidated. The functional PrPc can undergo a conformational change (the exact mechanism is also not fully elcudiated) altering it to the infectious prion state (dubbed PrPSc). The conformational change is initiated by contact of PrPSc with PrPc. The basic reaction scheme is listed below.

PrPc + PrPSc → 2PrPSc

Just one inital infectious protein, PrPSc, could be enough to transform all native PrPc. While the main transformation method requires PrPSc, it is not fully understood how the first PrPSc is formed; the twist on the chicken or egg conundrum. Although there is evidence showing that cows that have ingested the brain matter of diseased cattle will also contract the disease, the question on how the formation of the inital PrPSc occurred is still unanswered.

If the conformation into the PrPSc form resulted in a minimal behavioral difference from PrPc, there probably would be little cause for concern. Unfortunately, this conformational change coincides with drastic functional changes, reinforcing a main staple of biochemistry that "form equals function".

Once formed, PrPSc begins to congregate extracellularly, forming amyloid plaques that will ultimately disrupt the normal function of the tissue. Amyloid plaque formulation results in transmissilbe spongiform encephalopathies (TSE), a lethal condition. The most notable disease caused by prions is "mad cow disease" due to past media attention. In humans, prions have been associated with Creutzfeldt-Jakob disease, Gerstmann-Straussler-Schninker syndrome, Fatal familial insomnia, sporadic fatal insomnia, Alpers syndrome and Kuru.

The NK Linked Lecture: DNA and the Brain

A lecture given by Dr. James Watson that was made possible by Authors@Google series. Dr. Watson comments on his role in the discovery of the DNA double helix and reports on some of the research being conducted at Cold Springs Harbor, of which he is The Chancellor (I assume this position is equivalent to the director).

Most notable quote of the lecture: " This century will see the coming together of psychology and biology in the way that the last century was the coming together of chemistry and biology."

Dr. Watson's lecture focuses on the genetic roots of autism. Autism being a neurological disorder, which the disease manifests via spectrum as opposed to "present/not present". Looking for phenotypic patterns present in the progenitors of autistic children, Dr. Watson comments on research where subjective mental state assessments have been gathered for autistic progenitors and then compared to the prevalence of autistic child births between these individuals. An example being that the average IQ for autistic progenitors is 112, when the over-all average is 100.

Here's where it gets tricky though. Another researcher, Simon Baron-Cohen, came up with the categories of the female mind and male mind (Which in my opinion is a very poor choice of names for these categories). Where the male mind is defined as a systemizer, an individual that is mathematics based, logical and the female mind is defined as an empathizer, an individual that is good at connecting with other individuals. I believe that the terms male and female mind need to go; just use empathizer and systemizer instead. This choice of nomenclature will just inhibit these findings by miring them in unnecessary politically correct battles. Aside from the poor nomenclature, Dr. Watson states, that two individuals who are assessed as systemizers (male-mind oriented) are more likely to have an autistic child.

This appears to make sense, that individuals with a phenotype to systemize as opposed to empathizing will produce offspring more prone to systemizing, assuming that empathizer-systemizer spectrum holds true. But what genetic or neurological reasons are there for these parameters to be mutually exclusive? I believe that I have encountered many people who I would categorize as both strong systemizers and empathizers. Furthermore, according to this theory, that autism can be described as an individual at the extreme systemizer end of the empathizer-systemizer spectrum,then there should also be examples of neurological disorders on the opposite end of this spectrum.

Although I found this lecture engaging, I believe that I need to read more of Baron-Cohen's research to fully understand his position.

Well, enjoy the presentation.