Signal Transduction in Autism

EXECUTIVE SUMMARY: A study published this past summer analyzed tissue extracts from 20 donated brains, half (10) of which came from autistic donors. Half (5) of those people had histories of regression --- that is, they started out developing normally, speaking and everything, but then they lost some of the skills they had gained.

The brain tissue extracts were analyzed using a technique I describe in the main body of this post, that tests for the presence of a certain enzyme (protein kinase A, here) by giving it an opportunity to react with a sort of dummy peptide that can't really do anything except sit there and let the enzyme (and only that enzyme) act on it, and then introducing antibodies that will "tag" the altered peptides with an enzyme that will change a solution's color under certain conditions. This allowed the researchers to measure the relative activity of the enzyme across subjects or across brain regions; a similar measure, but using antibodies to the enzyme itself, rather than to its product, was used to measure the amount of enzyme present in each extract.

Using this method, the researchers found differences in protein kinase A activity and expression only in the frontal lobes, and only between the autism-with-regression subgroup of the autism group and both the controls and the rest of the autism group.

Protein kinase A is involved in intracellular signaling; it's one of the signal-boosting enzymes that helps the cell react quickly to changes in its environment. It modifies other proteins, affecting their activity. Some of its targets are proteins involved in neurotransmission (signaling between brain and nerve cells) and long-term potentiation (reinforcing those connections between neurons that are frequently used). It's this latter process that the study authors think may be disrupted in regressive autism.
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SFARI News posted some time ago on a study published on August 31 in PLoS ONE, comparing the amount of a certain enzyme present in tissue extracts from different regions of the brain between deceased subjects with and without autism who had donated their brains to the National Institute of Child Heath and Development Brain and Tissue Bank for Developmental Disorders.

The enzyme in question is protein kinase A, which plays a hugely important role in the cell, helping mediate a process called signal transduction, through which the cell is able to react to its changing environment, or to signals from other cells. In signal transduction, a molecule from outside the cell (usually a hormone) attaches to a receptor outside the cell and causes the receptor to change shape, thus altering the part of the receptor that's inside the cell and triggering a chain reaction of changes in enzymatic activity within the cell.

Protein kinase A participates in one particular signaling pathway: the one involving a class of receptors called G proteins, which are actually clusters of several smaller proteins that split apart whenever something attaches to its extracellular binding site. The now-mobile subunits then go on to do other things in the cell, most importantly to activate* an enzyme responsible for turning adenosine monophosphate (AMP) into cyclic AMP, which works as a signaling molecule inside the cell.

(Here is a cartoon from Nature Publishing Group's Scitable website illustrating that splitting apart of the G protein after a signaling molecule binds to its associated receptor; I adapted the image somewhat to make it less busy)

(Cyclic AMP)

Cyclic AMP is part of a class of molecules called "second messengers," which are small molecules that can bind to, and either activate or inhibit, a wide range of enzymes. Also, the enzymes responsible for making these molecules are regulated by receptors on the surface of the cell, so that when a signaling molecule binds to the receptor, the enzyme gets switched on (in the case of adenylyl cyclase, which is what turns regular AMP into cAMP) and starts churning out second-messenger molecules, which then go on to tinker with their target enzymes. In this way --- by coupling receptor binding with synthesis of these second-messenger molecules --- the cell can amplify the signal it receives, allowing it to react more quickly to changes in its environment.(Cartoon showing signal transduction using cyclic AMP as a second messenger, taken from this community college's Anatomy & Physiology II webpage. You can see how a hormone binding to its receptor frees up the receptor-coupled G protein to exchange its GDP for GTP and then go off and --- depending on the hormone --- either activate or inhibit adenylyl cyclase, which either starts or stops churning out cAMP, which goes on to do lots of different things, like activating enzymes, telling the cell to secrete various things, opening ion channels, etc. The only thing I don't like about this cartoon is that it only shows one cAMP molecule as the output of all the running around happening in the cell membrane, when really cAMP is being continuously produced by every active adenylyl cyclase. So, what that looks like, relative to the amount of hormone coming to the cell from outside, is more like this other cartoon, down below) (See, look at the arrows coming out of that yellowish triangle. One arrow splits into five, then 25, then more than you can clearly see. This table from the Memorial University of Newfoundland's cell biology webpage lists the number of molecules affected by each step in a cAMP-dependent signaling pathway, from the one molecule changed when a single molecule of hormone binds to its receptor, to the 10,000 molecules changed by the time adenylyl cyclase starts producing cAMP).

Anyway, protein kinase A is one of the enzymes activated by cAMP binding to it, and it is also mostly a regulatory enzyme --- that is, it activates or deactivates other enzymes. Protein kinase A does that by transferring a phosphate group from ATP (a small molecule made up of a sugar, a nucleotide base and three phosphate groups) to certain amino acid residues on any of its target proteins.

What kinds of proteins does protein kinase A regulate? Well, that depends on what kind of cell all this is taking place in. Every cell in the body contains a complete human genome; the differences between cell types are differences in which genes are expressed --- i.e., which proteins are present. So each cell type is going to have a different mix of proteins whose activity needs to be coordinated.

Some of its targets are proteins expressed in almost every cell type: these include a histone, one of a large family of proteins whose function is to condense chromosomal DNA that is not actively being transcribed or replicated; transcription factors (most notably, from the CREB family); a metabolic enzyme involved in storing energy for later use; ion channels; and other kinases (enzymes that alter the activity of other proteins by transferring phosphate groups onto them from ATP).

Although protein kinase A performs specialized functions in just about every cell type, I'm only going to talk about what it does in the brain, since that is the cell type relevant to this post. There, in addition to the stuff mentioned above, protein kinase A 1) helps regulate the synthesis of a common precursor to a variety of neurotransmitters, 2) helps form synapses by guiding the specialized proteins that allow the membranous sacs that deliver neurotransmitters from one neuron to the next toward the tip of the developing axon, and 3) with another protein kinase, regulates the ion-channel activity of the NMDA receptor, which is involved in strengthening the more frequently-used conntections between neurons. There may be more, but this is what I've been able to find.

For all that background information, the experiment I'm going to describe is actually pretty simple: like I said above, the researchers took tissue samples from five different regions of donated brains from autistic and non-autistic subjects, homogenized them (basically, ran them through a blender) and tested each sample for protein kinase A activity. The test they used is called the ELISA (for Enzyme-Linked ImmunoSorbent Assay --- see why people would rather call it Eliza?), which is a plastic plate covered with small circular wells (0.7 cm across by 1 cm deep) with, in this case, short peptides containing either serine or threonine (the two amino acids to which protein kinase A can attach a phosphate group), anchored to the bottom. (ELISA is most often used to test for the presence of antibodies --- that's how HIV testing is done --- so for that, the thing stuck to the bottom of the well would be the antigen to which whatever antibody you're testing for responds). They added their brain tissue extracts one by one to each well, along with a small amount of ATP dissolved in water (for the protein kinase to "borrow" phosphate groups from), then waited an hour and a half before emptying out the wells (the substrates, which were permanently affixed to the bottoms of the wells, would stay, along with, presumably, any phosphate groups that had been attached to them during the previous 90 minutes) and introducing an antibody specifically designed to bond with the phosphorylated form of the substrate peptide. Next, they washed the wells out thoroughly (to weed out everything that was not chemically bonded to the fixed substrates) and added a second antibody, chosen for its ability to bind to the first antibody, and which was also attached to an enzyme known for producing dramatic color changes as a side effect of its interaction with certain organic molecules. (A solution containing the molecule in question was also added, so that the wells in which the greatest proportion of the well-bottom peptides had been phosphorylated, and thus had the whole antibody rigmarole sticking off of them, would have the deepest color. There is even a way to measure color --- a device that can measure the degree to which something absorbs light at a given wavelength --- so that you don't have to rely on just your eyes to tell you whether this well or that one is a darker shade of yellow).

They used a somewhat similar technique, called Western blotting, to compare the amount of active protein kinase A between groups for each brain region. They injected their tissue samples from each of the different brain regions into a polyacrylamide gel, and ran an electric current through the gel to get the proteins to move through it. Since the gel resists having things move through it, different size proteins will travel through it at different rates. After a while, most of the proteins will separate themselves into bands along the gel, by size. Once this happened, the researchers transferred the proteins to a nitrocellulose membrane, and added antibodies specific to the catalytic (active) subunit of protein kinase A. Just like with the ELISA, there was also a secondary antibody coupled to a color-producing enzyme.

One thing that's a bit unusual in this study is that the researchers divided their brains from autistic donors into two groups, based on the developmental history of the donors. They had a "regressive autism" group, whose members started out developing typically but then lost some of the skills they'd acquired: speech was the most common skill that was lost, but some of the donors in this category also lost social skills and interest in social interaction. There was also a "non-regressive autism" group, whose members were delayed in language and social development from birth.

Subtyping autism is an increasingly popular thing for researchers to do, since "autism" is such a broad, flexible category that encompasses people with a very wide range of developmental and medical histories. It makes sense that researchers would want to subdivide this large, diverse group further to make sure they're comparing apples to apples when they look at different studies of "the autistic brain" or "the autistic immune system" or whatever.

The thing that's strange about subtyping in this study is that the number of brains being looked at is already so small. Each big group (autism, both regressive and not, and controls) had samples from ten people in it, and the researchers couldn't always get a sample from every point of interest on every brain, so sometimes the number of samples in a given category (brain region + donor neurotype) was less than ten; the smallest n for any category was 7. But that means that, with subtyping, the biggest n possible for either autism subgroup is 5, which looks more like a case study than a comparison across populations. But then, histological studies of donated brains always have to deal with smaller sample sizes, since there isn't exactly a superabundance of donated brains, and I guess if you have big differences among your subjects, you might as well sort them into subcategories, even if your subcategories are tiny.

At some point in this post I should probably mention the results of this study I've gone to such lengths to describe. The authors only found differences in protein kinase A activity in one region --- the frontal cortex --- and this difference was largest between one subgroup of the autistic group --- the autism-with-regression subgroup --- and both the non-regressive autism subgroup and the control group. The regressive autism subgroup had maybe a little less than half the PKA activity of the controls and the non-regressive autism subgroup (those two groups did not differ). Taken as a whole, the autism group had about 35% less PKA activity in the frontal-lobe samples than the control group.

The results were similar for the Western blot; the only region that showed any differences in PKA expression was the frontal lobe, and again, it was only the regressive autism subgroup that differed. Tissue extracts from that group had siginificantly less PKA in them than extracts from either the control group or the non-regressive autism subgroup; the unified autism group did not differ from the control group.

The researchers also looked for a correlation between their measure of PKA activity and various possible confounding factors, like how long each donor had been dead, the age of the donors when they died, whether they had any history of seizures, and what medications they were taking; they didn't find any relationship between any of these things and either outcome variable. Their measure of PKA expression also involved measuring how much of another protein was present in each tissue extract, both because that protein is about the same size as PKA, and thus cannot be separated from it using electrophoresis, and also to have a protein whose expression is not expected to vary across groups with which to compare relative amounts of the protein that is expected to vary.

Here is a picture of the Western blot showing both PKA (top row) and the other protein, a structural protein called beta-actin (bottom row), from all tissue samples:(Figure 2A, in Ji et al., 2011 - samples from autistic donors are on the left, and subdivided into non-regressive and regressive subtypes. Controls are on the right. You can see that, in the bottom row, the blobs are all approximately the same size, indicating expression of beta-actin is more or less the same across groups. You can also see that the blobs in the top row are a lot thinner - one space has nothing at all in it - in the regressive autism group than they are in either the non-regressive autism group or the control group. It looks like PKA expression is a bit more variable within the control group than beta-actin is, though.)

So, for a couple of reasons --- the extreme smallness of sample size, and also the degree of variation in PKA expression within the control group --- I am a bit skeptical as to whether this finding will hold up. It definitely needs to be tested a few more times, with bigger donor pools.

Leaving that aside, though --- what are the implications of this finding, should it be substantiated? The study authors refer to earlier literature that describes a role for cAMP signaling pathways in both brain development (obviously germane to a study about developmental disability) and long-term memory formation and learning (relevant to the question of how people can lose skills they once had). But it's not clear yet exactly what that role is; if you search for "protein kinase a brain" on BioNOT (a database of negative experimental results), you find an article claiming to find no difference in PKA activity between tissue samples taken from donors with Alzheimer's disease and those taken from healthy donors. So that complicates things a bit, as Alzheimer's is, even more than regressive autism, characterized by a loss of learned skills and memories.

Sources:
Ji, L., Chauhan, V., Flory, M., & Chauhan, A. (2011). Brain Region–Specific Decrease in the Activity and Expression of Protein Kinase A in the Frontal Cortex of Regressive Autism PLoS ONE, 6 (8) DOI: 10.1371/journal.pone.0023751

*What does it mean to activate an enzyme? Well, an enzyme is a kind of protein, and like all proteins, it has a range of three-dimensional configurations** it can assume, and only some of these possible shapes leave the binding site for the molecule the enzyme acts upon freely accessible. So when an enzyme is in one of those arrangements, and molecules of its particular substrate can just drift along and come into contact with the binding site(s), that's when the enzyme can be considered active. Binding of a phosphate group or some other small molecule at a different binding site will usually trigger a shape change; that is how enzymes can be activated or deactivated by other enzymes.

**I have this idea that proteins are called proteins just because of this shape-changing ability they have, in which they resemble the mythical Proteus.

On Falsifiability

"You can't prove a negative."

This statement gets tossed around a lot in arguments, especially arguments that lend themselves to the more abstract and theoretical planes, like "Does God exist?" or "Are we alone in the universe?" In those contexts, it's perfectly true --- you can't establish, once and for all, that X (whatever elusive entity X might be) doesn't exist.

A similar precept goes, "Absence of evidence is not evidence of absence."

But if it's true that you can't prove a negative, why is science news so regularly coming out with stories announcing such proofs? "Danish researchers find no link between thimerosal and autism," say, or "Mozart's music does not make you smarter," or "[G]iving up caffeine does not relieve tinnitus" --- all of these statements imply that something has been shown not to be the case.

I think the difference between those statements and the kind of "proving a negative" that's supposed to be impossible lies in how the questions are phrased. For a hypothesis to be testable, it has to have a set of conditions that must also be true --- and are measurable --- if the hypothesis is true. If you can make a prediction based on your hypothesis --- say, that if it's true that thimerosal in vaccines causes autism in children, then autism rates among school-aged children should fall as people stop using thimerosal in vaccines --- and if that prediction's failing to come true necessarily means your hypothesis was wrong, you can falsify the hypothesis. Based on what happens, your hypothesis can be proved wrong or right.

There's nothing inherently impossible about proving that a hypothesis is not true; usually, the statements that cannot be disproven are so vague, or deal with such a vast array of possibilities (i.e., "Space aliens exist somewhere in the universe") that there's no way to test them.

What Is Empathy?

I've thought for a while now that the concept of "empathy" most commonly used when talking about autism is excessively narrow.

Autistics --- especially Asperger's autistics --- are often said to lack empathy, which usually means two things: we can't infer a person's emotional state from their facial expression, body language, tone of voice or whatever other indirect cues they may be sending out, and we don't respond emotionally to other people's emotions, even when they are clear to us.

Here's Simon Baron-Cohen's definition of empathy, taken from the first chapter of his book The Essential Difference: Male and Female Brains and the Truth about Autism*:

Empathizing is the drive to identify another person's emotions and thoughts, and to respond to them with an appropriate emotion. Empathizing does not entail just the cold calculation of what someone else thinks and feels (or what is sometimes called mind reading). Psychopaths can do that much. Empathizing occurs when we feel an appropriate emotional reaction, an emotion triggered by the other person's emotion, and it is done in order to understand another person, to predict their behavior, and to connect or resonate with them emotionally.

In a later chapter, Baron-Cohen breaks the act of empathizing into two parts: a "cognitive component," in which you infer another person's likely mental state, and an "affective component," in which you feel something in response to what you either perceive or infer another person to be feeling. (Baron-Cohen gives an example of a homeless person standing in the street on a cold day, and people who see him being moved to feel a range of emotions: pity, guilt, or even anger at a political and economic system that allows such poverty to exist within a wealthy nation).

This two-fold conception of empathy grows out of an earlier idea, which Baron-Cohen has also written about: Theory of Mind. Theory of Mind seems to be more or less equivalent to the cognitive component of empathy described above:

A full-fledged theory of mind ... requires a representational system. This permits the representational mapping of others' emotional states in a manner that is different from picking up their emotions directly. For instance, an intention can be mapped onto a representational emotional topology, going from "the fox is chasing the chicken" (goal-directed) through "the fox is trying to catch the chicken" (intentionality) through "the fox wants to eat the chicken" (motivational) to "the fox is chasing the chicken and trying to catch it because it is hungry and wants to eat it" (emotional). Similarly, for the chicken: it is running (goal-directed) away from the fox (intentionality) because it is afraid (emotional) of being eaten (motivational).

As you can see here, there's a lot of different things feeding into a Theory of Mind. It's not just answering the question "What are they thinking/feeling?" --- that question can be further broken down into a whole string of smaller questions, as with the fox and chicken example above.

I also think that, for each step in that modeling process, there are two very different tasks involved in attributing a motive to another sentient being: first, you have to use your imagination to come up with a range of possible explanations for their action, and then you have to judge which explanation seems most likely. To do that, you draw both on what you actually know about the person and hir circumstances, but also on a general idea of what most people are like, and what most people would do in that person's shoes. (Or, if it's an animal whose behavior you hope to explain, you draw on whatever general knowledge you might have about that kind of animal).

It's in this stage that an alternative explanation for differences in empathizing begins to suggest itself: people from radically differing circumstances are going to have radically differing ideas of what most people would do in a given situation. Class and race are some obvious potential confounds here: middle-class white people are often at a loss to explain the actions of poor people of color, so they fall back on explanations that don't tax their imaginations too much --- i.e., those people are just stupid, lazy, criminal etc.

Gender also enters into it --- feminists have addressed this in their calls for a "reasonable woman" standard in law.

Given this, it shouldn't be too big a leap to suggest that some autistics might have trouble predicting how non-autistic people will react because they've figured out that their own responses to things are vastly different from most non-autistic people's responses. Thus, most of the time just putting oneself in another's shoes is not enough; one also has to imagine one's self greatly altered. This is hard to do, and without a whole lot of knowledge of a range of NT personalities and temperaments, you still won't have anything to put into your mental simulation where you used to be.

Several other autistic bloggers have made this point: that the empathy barrier goes both ways, and arises not from autistic insensitivity to emotion in general, but from the wildly divergent ways in which autistics --- and other neurological minorities --- and NTs experience emotion in the first place.

Like Bev says,

Autistic empathy is different from what the typical person experiences. It is no less real, no less deep or emotional. And I would argue that it's no less useful to society. Some people give hugs; others get the tissue.

Conversely, autistics are often perfectly adept at reading the emotional or intentional content of other autistics' "meaningless" behavior, because the mental state of the other autistic is likelier to be one they've experienced themselves.

*I've already posted about the problems I have with this theory of autism, so I won't revisit them here. I use his conception of empathy because I think it's the one

"The Next Step in Evolution"

(Cross-posted to Turner & Kowalski)

Over at John Elder Robison's blog, there's a two-part guest post on what it's like to be a woman with Asperger's. The guest blogger's name is Deborah McCarthy, and she is 49 years old, a vegan, an animal-rights activist, a Christian, and lives in Oregon.

While most of her writing just deals with her own experiences, particularly the differences she's identified between the way she thinks, feels, and perceives the world and the way most people do (and therefore often expect her to be that way, too), there are a couple of instances where she decides to make general pronouncements about things she really doesn't understand all that well. The statements she makes are inflammatory, hurtful (one more than the other, but neither is totally innocuous) and scientifically illiterate on a grand scale.

First, there's this:

Everybody says Asperger's' main symptom is a lack of empathy but I don't think that's true. Women exhibit differently from men. I'm sure conditioning has a lot to do with it but also women are predisposed from birth to be more empathic I think. I know I cry at the news very often. So I wanted to look at this and other characteristics to get clear on just what I can claim as mine and what just doesn't belong.

Empathy - I'm extremely empathic when it comes to the underdog, animals, children, the poor, the starving, etc. I have no sympathy whatsoever for the obese. Maybe that's from being bullied by my huge family members I don't know. Probably contributed. But for me it symbolizes greed and selfishness at the expense of another. After all, you don't get fat from veggies, you get fat from the flesh and mother's milk of another. Taking what doesn't belong to you. Taking more than your share. Taking more than giving. I have issues regarding fat. I admit it. Try not to hate me for it. I'm just being honest.

There are a lot of things wrong here, but since Sarah has already dealt with this part of the essay I will be brief, and stick to what is factually wrong with this paragraph, since Sarah focused on the failure of empathy involved. (Yes, I noticed the irony in such a massive display of bigotry cropping up as its author is trying to argue that autistics are fully capable of empathy. As they say at Shakesville, *lolsob*).

First: demographically speaking, poor women in America are much likelier than their richer counterparts to be obese. (The picture isn't as clear for men: some studies find that men of all classes are equally likely to be fat, while other studies find a relationship between low socioeconomic status and higher body weight that's significant, if not as pronounced as the corresponding trend among women). Second, it is possible to be fat and malnourished. We've all heard about how various systemic factors (agricultural subsidies making starchy, fatty, processed foods cheaper than produce and whole grains; lack of access to well-stocked grocery stores; lack of time to cook healthy meals, etc.) mean poorer people (who, as I mentioned, are fatter overall than richer people) tend to get a lot fewer nutrients out of their food, even when they're getting enough calories. There are also --- yes, even in the U.S. --- people so poor they can't always afford enough food. And, when bodies aren't getting enough energy, nutrients and raw materials (i.e., sugars, proteins, fats, starches), they start changing their metabolism to compensate for the scarcity. They become thriftier, hoarding more and more of the food they consume as fat.

As Kate Harding puts it:

Poor people are a lot more likely to go through cycles of eating too few calories followed by bingeing --- which, when it's known as "dieting," instead of "only being able to afford enough food sometimes" --- has indeed been shown to make people fatter in the long run.

You also cannot extrapolate whether someone is a meat-eater from their degree of fatness. There are fat vegans and vegetarians, and there are rail-thin omnivores. You can't look at someone's body and reliably predict what they eat. There are too many variables at work for there to be such a cut-and-dried relationship.

And attempting to judge a person's moral character by the shape of hir body? That belongs in the intellectual trash bin with all the earlier pseudosciences conceived along such lines.


Anyway, on to the second thing I found deeply problematic:

I, and others, don't feel that Asperger's is a disorder. I feel it is a neurological difference. You can SEE the difference on a brain scan. We are literally hard-wired differently than a neuro-typical person. (How many times have I said I'm just not wired that way!!) I believe we are a leap in evolution. Leaps like this occur in nature all the time. I believe a more childlike and pure sort of human is on the horizon. One that is less caveman-like and more angelic-like. More ethereal, less dense.

This idea --- that evolution is a linear progression from simple to complex, or primitive to advanced, "caveman" to "angel" --- is very common, but wrong.

The outcome of evolution is not any one species; it's biodiversity itself. It's change in populations over time. Individual variations arise, natural selection acts on them; organisms either propagate their genes or they do not. Intelligence, morality, free will --- or any other objective Good you might be tempted to see (human) evolution as trending toward --- doesn't enter into it.

Evolution is also not hierarchical. Every kind of creature that exists now is equally "evolved," and each constitutes an equally viable solution to the particular bio-engineering problems that shaped its unique evolutionary history.

In other words, there is no Great Chain of Being.

Finally, evolution is not a succession of different attempts to solve the same problem; it's a succession of solutions to a succession of problems. The natural environment is not static: climates shift, continents move, mountain ranges rise up and are worn down, natural barriers isolating potentially interbreeding populations from each other arise or disappear. The selective pressures that act on one generation won't be exactly the same as the pressures that will act on the next generation.

Here's a relatively simple explanation of what evolution is from my college introductory-biology textbook (Biology, Sixth Edition, by Neil A. Campbell and Jane B. Reece):

In the Darwinian view, the history of life is like a tree, with multiple branching and rebranching from a common trunk all the way to the tips of the youngest twigs, symbolic of currently living organisms. At each fork of the evolutionary tree is an ancestor common to all lines of evolution branching from that fork. Closely related species, such as the Asian elephant and the African elephant, are very similar because they share the same line of descent until a relatively recent divergence from a common ancestor. Most branches of evolution, even major ones, are dead ends; about 99% of all species that have ever lived are extinct.

...

We can summarize Darwin's main ideas as follows:

Natural selection is differential success in reproduction (unequal ability of individuals to survive and reproduce).

Natural selection occurs through an interaction between the environment and the variability inherent among the individual organisms making up a population.

The product of natural selection is the adaptation of populations of organisms to their environment.

Thus, there are as many outcomes of evolution as there are ecological niches to be filled.

I also like this image of a circular Tree of Life, in which all currently-extant taxa (er, categories of organisms, for the nonbiologists reading!) radiate out from the single hypothesized common ancestor of all. It conveys the never-ending, multifarious nature of evolution much better than any other drawing I've seen.

It will probably not strike regular readers of this blog as news that such a teleological, hierarchical view of evolution has acted as (pseudo-)scientific justification for race- and class-based oppression. This thread has been particularly noticeable in the history of racism: people of African descent have historically been seen as ape-like and "primitive" (i.e., less evolved, less civilized, certainly incapable of governing themselves without white people running the show for them!) by white people.

While I'm not really worried about autistic people oppressing neurotypicals --- we don't have the numbers or the political power or social privilege to do so systematically, although individual autistic chauvinists can, and do, loudly proclaim their neurological superiority on the Internet --- this kind of "Aspie-supremacist" rhetoric valorizing the Vulcan-like, superintelligent-but-socially-naive autistic person can further marginalize autistic people who don't fit that mold. If the autistic-rights movement embraces the "Aspie" to the exclusion of other autistic points of view, then other types of autistics will be right where they were before neurodiversity: voiceless and unnoticed.