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Autism Treatment - New technologies give hope to patients
New molecular technologies lead to new findings and possible treatment concerning Autism.

Autism is a neurological development disorder causing impaired social interaction and communication and restricted repetitive behavior. Its origins and causes have long been debated, but only recently has there been any real data to suggest a possible underlying pathology on the cellular level. The cause of autism still remains uncertain, showing a strong genetic component, but the genetics of autism have proven to be very complex and difficult to tackle. In some cases, autism has been attributed to agents that cause birth defects, such as heavy metals, pesticides and certain mutagens. Some have even proposed vaccination as a possible cause for autism, although this has yet to be proven or show any real scientific basis. Whatever the cause, autism remains a big scientific and medical challenge. The diagnostic spectrum of Autism has three distinct branches, with symptoms usually surfacing before the age of three. The array of symptoms is highly diverse, and as some research suggests, the causes themselves could be. An autism related culture has developed, with some individuals striving to find a cure or treatment for such individuals, and others stating that it is not a disease to be cured and people suffering from autism should be embraced an integrated into social systems.

Recent research done by the Mitochondrial and Metabolic Disease Center at the University of California, San Diego School of Medicine might shed some light on the mechanism of this disease and give hope for a future treatment or even a cure. Testing a new theory, the researchers have found that a century old drug, used to combat African sleeping disease, might just be the substance to cure autism.

Tens of UC San Diego scientist and skilled researchers from diverse areas have banded together to work on, and discover, a unifying mechanism to explain and possibly cure autism. Compiling a completely new theory using antipurinergic therapy Dr. Naviaux and colleagues have purposed a unifying mechanism explaining how the different causes, both genetic and environmental, affect the onset of autism by causing a sustained cell danger response, an innate metabolic cellular mechanism responsible for cellular immunity and inflammation.

“Our cell danger theory suggests that autism happens because cells get stuck in a defensive metabolic mode and fail to talk to each other normally, which can interfere with brain development and function. We used a class of drugs that has been around for almost a century to treat other diseases to block the ‘danger’ signal in a mouse model, allowing cells to return to normal metabolism and restore cell communication.” - says Robert Naviaux, M.D. “When cells are exposed to classical forms of dangers, such as a virus, infection, or toxic environmental substance, a defense mechanism is activated. This results in changes to metabolism and gene expression, and reduces the communication between neighboring cells. Simply put, when cells stop talking to each other, children stop talking.”
Considering mitochondria are the key players in cellular signaling and infectious and noninfectious cellular stress, innate immunity, and inflammation, the researchers first searched for a common cellular marker that was critical for immunity responses and linked to mitochondria. They found several, including adenosine triphosphate, a molecule with a very diverse metabolic role, and many other mitokines, molecules produced by mitochondria in distress. These mitokines have a high range of metabolic functions inside the cell, but a very different one outside of them. Up to fifteen different purinergic receptors on the surface of several classes of cells can be affected by these mytokines, which in turn controls a broad range of biological functions, up to 15 different functions, relating to autism.

The researchers tested many substances, among them suramine, which has been used for nearly a century to treat African sleeping disease, and found that the signal inhibitory function of suramine corrected autism-like symptoms in model organisms, mice with a form of autism. The drug restored 16 types of multiple abnormalities including normalizing brain synapse structure, cell-to-cell signaling, social behavior, motor coordination, and normalizing mitochondrial metabolism. Moreover, the drug prevented cerebellar Purkinje cell loss, correction of the ultrastructural synaptic dysmorphology, and correction of the hypothermia, metabolic, mitochondrial, P2Y2 and P2X7 purinergic receptor expression, and ERK1/2 and CAMKII signal transduction abnormalities.

Doctor Naviaux said: “The striking effectiveness shown in this study using APT to ‘reprogram’ the cell danger response and reduce inflammation showcases an opportunity to develop a completely new class of anti-inflammatory drugs to treat autism and several other disorders. Of course, correcting abnormalities in a mouse is a long way from a cure for humans, but we are encouraged enough to test this approach in a small clinical trial of children with autism spectrum disorder in the coming year. This trial is still in the early stages of development. We think this approach offers a fresh and exciting new path that could lead to development of a new class of drugs to treat autism.”

Findings published in the March 13 issue of PLOS ONE in an article titled “Antipurinergic Therapy Corrects the Autism-Like Features in the Poly(IC) Mouse Model.”
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Interesting research. In addition to it, when a fetus is not delivered by one to two weeks past full gestation or when the need is medically indicated, doctors will deliver babies by inducing or augmenting labor, often with the drug pitocin. This policy is followed in order to improve the successful outcome of the birth and to preserve the health of the mother. However, a new study has found, “Children of women who had labor induced or sped up with drugs were more likely to go on to develop an autism spectrum disorder.”
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The best medication for attention deficit disorder Inattentive (ADHD-PI) or Inattentive ADD is maybe not stimulant. There ar some psychiatrists that believe that Inattentive ADD or attention deficit disorder-PI might not be attention deficit disorder in the slightest degree which patients with this sub type of ADHD might respond whole otherwise than the opposite sub types to stimulant medication.
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