Enter another peptide, neurokinin A, into the field and an interesting report published in December 2011 by Mostafa and AL-Ayadhi* (full-text). Before getting into the nitty-gritty of the content and possible meaning, it is interesting to note that this is the same team who quite extensively published on autism last year (2011) and in particular, those quite peculiar findings in relation to low levels of progranulin.
Aside from being a peptide, a neuropeptide, neurokinin A has an interesting role in the mechanism of inflammation, as part of their family trade (the tachykinins). It is with this in mind, that the authors set out to study this peptide and turned up some interesting results:
- Serum levels of neurokinin A and anti-ribosomal P protein antibodies were measured for 70 children diagnosed with an autism spectrum condition and 48 age- and sex-matched asymptomatic controls. I can't really offer a very intellectually satisfying account of what anti-ribosomal P protein antibodies are, aside from the fact that they have been noted in autoimmune conditions such as systemic lupus erythematosus (SLE) and elevated titers (levels of antibodies) have been noted during lupus psychosis.
- As a group, participants with autism showed significantly higher levels of serum neurokinin A than controls. Based on CARS criteria, specifying autism presentation as mild/moderate or severe, participants with a more severe autistic presentation presented with much greater group levels of neurokinin A than those judged mild/moderate.
- Anti-ribosomal P protein antibodies were present in around 40% of participants with autism although I can't find anything in the paper which provides comparative data on control participants. The authors also suggest that there was a significant correlation between levels of neurokinin A and anti-ribosomal P protein antibodies (r=0.34, p=0.004). Not being one to quibble, the data does look rather messy from my angle (see figure 2) and r=0.34 is not, it has to be said, that good a value of correlation given that CARS and neurokinin A levels correlated by r=0.62 [r=1 = perfect correlation].
On the basis of their presented data, I would tend to suggest that the neurokinin A findings are probably the more exciting results included in this paper and certainly provide some interesting fodder for further study. Non-neuronal cell production of the tachykinins seems to be a focus of the paper and an interesting suggestion that exposure events to various environmental factors (food, pollutants, etc) might trigger the production of neurokinin A from immune-related cells.
Another interesting perspective to all this is the role of neurokinin A (and other tachykinins such as substance P) on airway disease such as asthma. No data is provided in the current paper on the rates of respiratory symptoms in their patient group (breathlessness, wheeze, coughing) aside from exclusion of participants with 'allergic, inflammatory or autoimmune disorders' or those 'receiving any medications' so we can only speculate on any connection. Certainly my previous posts on asthma and autism and airways and autism perhaps direct some attention to a possible connection between elevated neurokinin A and cases where respiratory comorbidity might be present, the other side of which may need to look at whether neurokinin A levels correlates with autism severity correlates with airway symptoms?
To end, a little classic Smiths.. what a charming man.
* Mostafa GA. & AL-Ayadhi LY. The possible link between the elevated serum levels of neurokinin A and anti-ribosomal P protein antibodies in children with autism. Journal of Neuroinflammation. December 2011.