Levels of Bcl-2 and P53 are altered in superior frontal and cerebellar cortices of autistic subjects

Cell Mol Neurobiol. 2003 Dec;23(6):945-52. doi: 10.1023/b:cemn.0000005322.27203.73.


1. Autistic disease (AD) is a severe neuropsychiatric disorder affecting 2-4 children per 10,000. We have recently shown reduction of Bcl-2 and increase in P53, two important markers of apoptosis, in parietal cortex of autistic subjects. 2. We hypothesized that brain levels of Bcl-2 and P53 would also be altered in superior frontal cortex and cerebellum of age-, sex, and postmortem-interval (PMI)-matched autistic subjects (N = 5 autistic, N = 4 controls). 3. Brain extracts were prepared from superior frontal cortex and cerebellum and subjected to Western blotting. 4. Results showed that levels of Bcl-2 decreased by 38% and 36% in autistic superior frontal and cerebellar cortices, respectively when compared to control tissues. By the same token, levels of P53 increased by 67.5% and 38% in the same brain areas in autistic subjects vs. controls respectively. Calculations of ratios of Bcl-2/P53 values also decreased by 75% and 43% in autistic frontal and cerebellar cortices vs. controls respectively. The autistic cerebellar values were significantly reduced (p < 0.08) vs. control only. There were no significant differences in levels of beta-actin between the two groups. Additionally, there were no correlations between Bcl-2, P53, and beta-actin concentrations vs. age or PMI in either group. 5. These results confirm and extend previous data that levels of Bcl-2 and P53 are altered in three important brain tissues, i.e. frontal, parietal, and cerebellar cortices of autistic subjects, alluding to deranged apoptotic mechanisms in autism.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Autistic Disorder / genetics
  • Autistic Disorder / metabolism*
  • Autistic Disorder / pathology
  • Cerebellar Cortex / metabolism*
  • Cerebellar Cortex / pathology
  • Frontal Lobe / metabolism*
  • Frontal Lobe / pathology
  • Humans
  • Male
  • Proto-Oncogene Proteins c-bcl-2 / genetics
  • Proto-Oncogene Proteins c-bcl-2 / metabolism*
  • Statistics, Nonparametric
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism*


  • Proto-Oncogene Proteins c-bcl-2
  • Tumor Suppressor Protein p53