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



 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


       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


       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


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

 Cerebral Cortex and Basal Forebrain,” is posted on the Web at under the July issue.

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