Zoonostic infections (shared by animals and humans) that have come to be understood in the scientific community as prion disease have in turn created research implications for a variety of degenerative neurological illnesses which have similarity in symptoms. Some diagnostic findings for the prion type diseases include atrophy, neuronal loss, and presence of amyloid plaques.
Some prion diseases are mad cow disease, known as Bovine Spongiform Encephalopathy (BSE) and Creutzfeldt Jakob Disease (CJD), a human form of the Transmissible Spongiform Encephalopathies (TSE). Current research into what has come to be understood as prion disease will hopefully result in answers to questions about how to treat neurologically degenerative diseases overall, including cases of autism.
Some (link) question the currently held theory that misfolded and gene-less proteins (prions) - that are late occurring in the duration of transmissible spongiform encephalopathy illness - represent initial cause of neurodegenerative illnesses. Even Heino Dringer, who pioneered understanding with regard to the nature of prions, has felt that "it will turn out that the prion concept is wrong". It appears that many animals that come down with Transmissible Spongiform Encephalopathy never even have evidence of misfolded proteins, but do have evidence of bacterial DNA.
Is it that the pathologic prions are actually a later result, from an initial infectious process involving filterable forms of M avium, M bovis, and M tuberculosis bacteria? These are represented as having pleomorphic properties; a plasticity to assume many forms, some viral-like and different from their classical parent. If it is true, that the trickier bacteria morph in an as yet to be entirely understood infectious process that in turn result in amyloid plaque and latent pathologic prion - then one researcher proposes antitubercular drugs might help in cases of neurodegenerative illnesses.
The detection of 14 - 3 - 3 protein, in the cerebrospinal fluid, originally thought to be a highly reliable indicator for prion diseases, also appears in CNS tuberculosis and the very fabric of the TSE's and prion diseases, amyloid has been implicated and re-implicated as being caused by bovine and human tuberculosis. (source link)
There is an ongoing study (last updated in 2008) with regard to treating children with autism, with D-cycloserine, an antitubercular drug - in order to reduce certain autistic features. There is a study that is still recruiting participants, also using D-cycloserine for remediation of schizophrenia.
Cycloserine is an antibiotic effective against Mycobacterium tuberculosis. For the treatment of tuberculosis, it is classified as a second line drug, i.e. its use is only considered if one or more first line drugs cannot be used. Although in principle active against other bacteria as well, cycloserine is not commonly used in the treatment of infections other than tuberculosis. (link)
In the ongoing process of learning about prion disease the following have also been written...
I have a daughter, labeled autistic at three years of age, and then labeled with schizophrenic tendencies at ten years of age - who compels my meanderings and attempts to understand neurological illness.