you should be ashamed of yourself bioI.. but you got me anyway..

Marijuana is also asserted as a minor risk factor. But correlation is not causation, so it might be that schizophrenics have certain mental charecteristics (long before getting recognizable schizophrenia) that cause them to be somewhat more likely to use marijuana. In the case of genes, correlation is causation only because it is virtually certain that getting schizophrenia can't change someone's genes. 
If you look at that literature closely it looks a lot like the marijuana/schizophrenia thing is analogous to the hemophiliac gettings shot in the wrist. Some percentage of the population that is already at risk really really needs to stay off the chronic.

How does schizophrenia with onset in your mid-20s affect fitness? Hasn't most of the world reproduced by then? 
 
Where do you get the statistics for families dwindling away? Is it the same for autism?

Matt -  
Jay Gingrich has some work that speaks to the florid hallucinations: 
http://www.nature.com/nature/journal/v452/n7183/abs/nature06612.html 
Here we show that the mGluR2 interacts through specific transmembrane helix domains with the 2AR, a member of an unrelated G-protein-coupled receptor family, to form functional complexes in brain cortex. The 2AR–mGluR2 complex triggers unique cellular responses when targeted by hallucinogenic drugs, and activation of mGluR2 abolishes hallucinogen-specific signalling and behavioural responses. In post-mortem human brain from untreated schizophrenic subjects, the 2AR is upregulated and the mGluR2 is downregulated, a pattern that could predispose to psychosis. 
 
Whatever happened to DISC1?  
we report that individuals in a discordant twin sample with a DISC1 haplotype, associating with schizophrenia as well as working memory impairments and reduced gray matter density, were more likely to show deficits in sociability than those without the haplotype. Our findings demonstrate that alterations in DISC1 function during brain development contribute to schizophrenia pathogenesis. 
 
I'm thinking that studying particular Sz symptoms is going to be more fruitful than the whole disease, but Greg's larger point makes me despair of ever modelling schizophrenia in any satisfactory way. Treatment might be restricted to new ways to alter dopamine cycling.

how and when to integrate GWAS / hapmap data into these?  
 
no mention of ben g's fave being associated with iq for instance..

fly -  
 
i worry about the neocortex. during development an initial set of stemcells differentiates into radial glia and neural progenitors. the neural progenitor gets its 'cellular identity' and position in the circuit by being born after a certain number of cell divisions and at a certain spot on the ventricular zone. the newborn neurons climb up radial glia to their spot close to the developing skull surface.  
 
one concern is that radial glia may not know how to be big enough to reach from the ventricular zone to the skull of an adult. 
 
another concern is the surgical precision it would take to stick a dot of neural stem cells in the right spot.  
 
point is there isn't anything like a niche anywhere terribly accessible to where adult neocortical neurons are hanging out. 
 
but i'm down for all the stuff besides brain mods. since i don't know how complicated those places are i assume it'll work. :)

I happened to listen to this tonight while I was cleaning my apartment and I was struck by how much emphasis one of the authors put on language as the true defining characteristic of Arabs. I thought "Isn't it an ancestry first and foremost?" Then I realized I didn't know. I checked out wikipedia and it def seems this guy was pushing a language agenda.  
 
Anyway, I know there is a lot of research concerning the influence of genetics on universal characteristics of language, but is there much known about variation in language? Given the age of the major language splits, would there be specialization as far as language styles are concerned?