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    Nicotine and Autism

     Nicotine Receptors May Play Role In Development of Autism

     Cholinergic nicotinic receptors, which have become a hot area for brain

     researchers, are linked to yet another psychiatric-neurological

     disorder—autism.

     

     By Joan Arehart-Treichel in Psychiatric News, July © 2001 American

     Psychiatric Association.

     

           Deep inside the human brain, cholinergic nicotinic receptors are busy

     plying their trade, and one might view them as triple agents. They release

     the nerve transmitter acetylcholine from certain nerve ends, they receive it

     at others, and they can be stimulated by nicotine—yes, from cigarette

     smoking!

           Even more intriguing, these receptors have been implicated of late in

     a spate of psychiatric and neurological disorders such as Alzheimer’s

     disease, Parkinson’s disease, schizophrenia, and Tourette syndrome

     (Psychiatric News, March 13, 2000).

           And now the receptors have been linked to yet another psychiatric- neurological condition—autism.

           The finding comes from Elaine Perry, Ph.D., of Newcastle General

     Hospital in Newcastle-Upon-Tyne, England, and her colleagues. It is reported

     in the July American Journal of Psychiatry.

           “This is an important paper,” Peter Whitehouse, M.D., Ph.D., a

     neurologist-psychologist with Case Western Reserve University in Cleveland,

     told Psychiatric News. “It is probably the first [neurochemical]

     investigation of cholinergic systems in autism. And the findings regarding

     the nicotinic receptors do suggest a potential role for them in the

     mechanisms of autism, particularly related to the ability to focus attention

     and to interact with other people.”

           During the past few years, there have been intimations that the nerves

     and other brain mechanics that concern themselves with acetylcholine—the

     so-called “cholinergic systems”—might be implicated in autism. For example,

     cholinergic neurons in the basal forebrain, an area of the brain known to be

     involved in attention, have been found to be abnormally plentiful, and

     abnormally large, in children with autism.

           As for a chemical known to influence the development and function of

     cholinergic neurons in the basal forebrain area—brain-derived neurotrophic

     factor—abnormally high levels of it have been found in the bloodstreams of

     newborns with autism. Thus, these and some other discoveries prompted Perry

     and her team to try to determine whether, and how, various cholinergic

     players conspire in the autism disease process.

           They acquired frozen brain samples from seven deceased adults who had

     had autism and from 10 deceased adults who had no mental disorder. They then

     examined the activities of specific cholinergic functions in the brain

     samples and compared the activity of each function in brain samples from the

     autistic subjects with the activity in brain samples from the control

     subjects.

           If any functions were found to behave abnormally in brain samples from

     autistic subjects, they reasoned, then those functions might well be

     culprits in the autism disease process.

           For instance, the researchers measured in the brain samples the

     activity of acetylcholinesterase, the enzyme that makes acetylcholine. They

     then compared the activity of the enzyme in samples from the autism group

     with the activity of the enzyme in samples from the control group. They

     found no difference. So they concluded that this particular enzyme is

     probably not implicated in autism.

           They also measured the activity of the enzyme that breaks down

     acetylcholine. They then compared the activity of this enzyme in samples

     from the autism group with the activity of this enzyme in samples from the

     control group. Again they found no difference. So they concluded that this

     enzyme, too, is not involved in autism.

           However, they did find something interesting regarding the chemical

     that is known to influence the development and function of cholinergic

     neurons in the basal forebrain—that is, brain-derived neurotrophic factor.

           They found three times more of the factor in the basal forebrain area

     of brain samples taken from autism subjects than in samples taken from

     mentally normal subjects. So they think that this factor might indeed be

     involved in autism.

           And they also found considerably less nicotinic receptor activity in

     the cerebral cortex of brain samples taken from autism subjects than in the

     cerebral cortex of samples taken from mentally normal subjects. So they

     believe that faulty nicotinic receptors might also be culprits in autism.

           Such findings, they concluded in their paper, suggest that “the role

     of the cholinergic system in autism should be investigated further. . . .”

           Also of interest, they wrote, is that the abnormalities they have

     detected in brain samples from autism subjects more closely resemble those

     in brain samples from schizophrenia subjects than those in brain samples

     from Alzheimer’s disease or Parkinson’s disease subjects. Such similarities,

     they believe, are not surprising since “there is an extensive overlap in

     clinical symptoms between autism and schizophrenia, both behaviorally and

     cognitively. . .and the same neural systems are likely to be involved in

     both, although differing in developmental staging and etiology.”

           But the findings by Perry and her team are especially provocative

     because they may point the way to an effective treatment for

     autism—something that does not currently exist. For instance, might nicotine

     or another drug that stimulates the nicotinic receptors possibly help autism

     patients? Perry thinks so. In fact, she told Psychiatric News, she would

     like to explore this possibility. The most recently approved drug for

     Alzheimer’s disease—galantamine—might also be able to counter autism,

     Whitehouse conjectures. The reason, he said, is that the drug is thought to

     be capable of influencing the nicotinic receptors (Psychiatric News, April

     20).

           The study, “Cholinergic Activity in Autism: Abnormalities in the

     Cerebral Cortex and Basal Forebrain,” is posted on the Web at

     http://ajp.psychiatryonline.org under the July issue.

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