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Males with Autism Have Fewer Cells in Brain’s Emotional Memory Hub

Science Update

Males with autism have fewer cells in a part of the brain that has a key role in emotion and memory, according to NIMH-funded researchers at the University of California, Davis. This study provides the first scientific evidence that it is the number of cells in the area of the brain called the amygdala that is affected by the disorder and not the density of cells or volume of tissue. Research results were published in the July 19 issue of the Journal of Neuroscience.

David Amaral, Ph.D., and Cynthia Mills Schumann of the U.C. Davis Medical Investigation of Neurodevelopmental Disorders (M.I.N.D.) Institute used modern techniques to study the three-dimensional structure of brain areas known to show differences in autism. Comparing the postmortem brain tissue of nine males who had autism to 10 males who did not, the researchers counted and measured representative samples of cells in the amygdala. Based on their current findings, the researchers aim to determine why there are fewer cells and whether other brain areas are similarly affected in autism.

Autism is a developmental disorder that causes severe and pervasive impairment in thinking, feeling, language, and the ability to relate to others. The disorder develops in childhood and generally is diagnosed by age three. Autism is about four times more common in boys than girls.1 Girls with the disorder, however, tend to have more severe symptoms and greater cognitive impairment.1,2

Schumann CM, Amaral DG. Stereological Analysis of Amygdala Neuron Number in Autism . Journal of Neuroscience. 19 Jul 2006; 26(29): 7674-7679.

1. Fombonne E. Epidemiology of autism and related conditions. In: Volkmar FR, ed. Autism and pervasive developmental disorders. Cambridge, England: Cambridge University Press, 1998; 32-63.

2. Yeargin-Allsopp M, Rice C, Karapurkar T, Doernberg N, Boyle C, Murphy C. Prevalence of Autism in a US Metropolitan Area. The Journal of the American Medical Association. 2003 Jan 1;289(1):49-55.