The mystery of madness

This morning I read an article in New Scientist that, as scientific articles tend to do, confirmed a previously unfounded belief of mine.

Kéri examined a gene involved in brain development called neuregulin 1, which previous studies have linked to a slightly increased risk of schizophrenia. Moreover, a single DNA letter mutation that affects how much of the neuregulin 1 protein is made in the brain has been linked to psychosis, poor memory and sensitivity to criticism.

[...]

People with two copies of the neuregulin 1 mutation – about 12 per cent of the study participants – tended to score notably higher on these measures of creativity, compared with other volunteers with one or no copy of the mutation. Those with one copy were also judged to be more creative, on average, than volunteers without the mutation.

Now, this is obviously a very new study, and as such shouldn’t be taken to confirm or refute anything yet. But its findings are so in line with what I’ve naively believed for years that I can’t help but jump on board.

Lately I’ve been reading a gross amount of Terry Pratchett books, as a feel-good kind of escape from the jobhunt, as a retreat from academic reading, and as a study in how to structure a novel. If you’ve ever read a Terry Pratchett book, then you probably see my point already. For those who haven’t, his books are so disjointed, with artful hairpin turns to crack a joke, and so off-the-wall with the subject matter, that the only reasonable reaction for a reader to have is: “This man’s brain is not right.” It simply must be broken somehow.

I believe that.

If you’re a Terry Pratchett fan, it also won’t come as news to you that he was recently diagnosed with early-onset Alzheimer’s. From his speech to the Alzheimer’s Research Trust Conference:

I’d like a chance to die like my father did—of cancer, at 86. Remember, I’m speaking as a man with Alzheimer’s, which strips away your living self a bit at a time. Before he went to spend his last two weeks in a hospice he was bustling around the house, fixing things. He talked to us right up to the last few days, knowing who we were and who he was. Right now, I envy him.

It’s a very moving speech, and I recommend reading it in full. But I find this tragic news intriguing because to me it confirms what I’ve always wondered about the man: that his brain operates fundamentally so differently that it could be called pathological.

Now, although I have no scientific background whatsoever, I do have Google Fu, and so I should say that it appears that at present the academic consensus is that there is no link in cause between schizophrenia and Alzheimer’s. From one such paper (available in full!):

This study provides evidence that elderly patients with schizophrenia showing Alzheimer’s disease neuropathology in the brain have increased levels of Aß0. Thus, cognitive impairment in these patients could be related to the dementia-associated amyloid ß-peptide pathogenicity in the brain. However, the larger group of elderly patients with schizophrenia, who were comparably demented but did not evidence Alzheimer’s-related histopathology, did not show significantly elevated levels of amyloid ß-peptide. Analysis of the total brain amyloid ß-peptide content in the present patient cohort showed that the occurrence of cognitive decline in the course of schizophrenia is distinct from the neuropathologic or molecular processes linked to amyloid ß-peptide in Alzheimer’s disease.

From what I’ve read, that basically means that schizophrenia is not considered to be related to Alzheimer’s in terms of cognitive impairment because different factors seem to be causing the impairment in each disease. It helps to read the Wikipedia entry on amyloid ß, which explains:

Amyloid beta (Aβ or Abeta) is a peptide of 39–43 amino acids that appear to be the main constituent of amyloid plaques in the brains of Alzheimer’s disease patients. Similar plaques appear in some variants of Lewy body dementia and in inclusion body myositis, a muscle disease. Aβ also forms aggregates coating cerebral blood vessels in cerebral amyloid angiopathy. These plaques are composed of a tangle of regularly ordered fibrillar aggregates called amyloid fibers, a protein fold shared by other peptides such as prions associated with protein misfolding diseases. Research on laboratory rats suggest that the two-molecule, soluble form of the peptide is a causative agent in the development of Alzheimer’s and that the two-molecule form is the smallest synaptotoxic species of soluble amyloid beta oligomer.

That’s about all I know so far, and I wanted to share. I realize like it might sound like I crudely accept the trade-off of having brilliant people suffer, as long as they keep making pretty things for me to passively enjoy. I don’t want to sign off on anyone else’s pain, but I would like to encourage a mindset of critically assessing what is called bad and what good, at least when it comes to brain function.

I don’t know how all this stuff works, but I guess that’s my point. I don’t even know if I want to understand it one day. At this point I feel I’d be better off just closing my eyes and gritting my teeth when I’m drawing the straw of reincarnation—or of aging, if there’s any difference.