Molecular NeuroscienceReduction in anti-apoptotic protein Bcl-2 in autistic cerebellumFatemi, S. HosseinCA; Halt, Amy R.; Stary, Joel M.; Realmuto, George M.; Jalali-Mousavi, MaryamAuthor Information Department of Psychiatry, Division of Neuroscience Research, University of Minnesota Medical School, Box 392, Mayo Bldg., 420 Delaware Street SE, Minneapolis, MN 55455, USA CACorresponding Author Received 21 November 2000; accepted 22 January 2001 NeuroReport: April 17th, 2001 - Volume 12 - Issue 5 - p 929-933 Buy Abstract Autism is a neurodevelopmental disorder with genetic and environmental etiologies. Neurohistologic findings have shown Purkinje cell depletion and atrophy in the cerebellum of autistic subjects. We hypothesized that apoptotic mechanisms might explain these Purkinje cell findings. Bcl-2 is a potent anti-apoptotic regulatory protein, which is reduced in schizophrenic brains. Autistic and normal control cerebellar cortices matched for age, sex and PMI were prepared for SDS-gel electrophoresis and Western blotting using specific anti-Bcl-2 antibodies. Quantification of Bcl-2 showed a significant 34–51% reduction in autistic cerebellum (mean (± s.d.) optical density/75 μg protein 0.290 ± 0.08, n = 5) compared with controls (0.595 ± 0.31, n = 8;p < 0.04); levels of neuronal-specific class III β-tubulin (controls 49.8 ± 6.7; autistics 36.2 ± 18.2), or β-actin (controls 7.3 ± 2.7; autistics 6.77 ± 0.66) in the same homogenates did not differ significantly between groups. These results indicate for the first time that autistic cerebellum may be vulnerable to pro-apoptotic stimuli and to neuronal atrophy as a consequence of decreased Bcl-2 levels. © 2001 Lippincott Williams & Wilkins, Inc.