The developing nervous system is particularly sensitive to teratogens and is the system least protected by present standards for safety testing. Research in this lab has focused on morphologic and functional expression of early injuries to the CNS. Recent investigations have included neuroendocrine effects of antimitotic agents and ethanol.

       The present focus in the lab is on the neurobiological origin of autism. This disorder can be caused either by exposure to toxic agents or by genetic abnormalities. We have proposed that the key to understanding how the same disorder can arise from disparate causes is that the timing of the injury to the embryo is the same in both cases. We know that the teratologic cases are due to insults during neural tube closure. Mutations of some of the early developmental genes active at the same time in the region of injury are good candidates for explaining familial cases of autism. The anatomical phenotype in humans is similar to that of mice transgenic for null mutations of several early developmental genes, and similar to that of a teratologically-induced animal model developed in this laboratory.

       Ongoing projects include comparing the anatomical details of the animal model to those of human cases and studying the connections of neurons in the brain stem of the animal model. In collaboration with the investigators from Rochester's Departments of Pediatrics and Neurology and The Hospital for Sick Children in Toronto, genomic DNA of patients with autism and their family members is being evaluated for mutations of early developmental genes. In collaboration with Cornell Medical College, the laboratory is investigating how the expression of early developmental genes is influenced by teratogens.

       This program has been designated as one of NIH's Collaborative Programs of Excellence in Autism. Mare information about this program is available through our special web site devoted to Autism Research at the U of R

Recent Publications

Stodgell CJ, Ingram JL, O’Bara M, Tisdale BK, Nau H, Rodier PM. Induction of the homeotic gene Hoxa1 through valproic acid's teratogenic mechanism of action. Neurotoxicol Teratol. 2006 Sep-Oct;28(5):617-624.

Devlin B, Cook EH, Coon H, Dawson G, Grigorenko EL, McMahon W, Minshew N, Pauls D, Smith M, Spence MA, Rodier PM, Stodgell C, Schellenberg GD. 2005. Autism and the serotonin transporter: the long and short of it. Mol Psychiatry. Dec;10(12):1110-1116.

Arndt TL, Stodgell CJ, Rodier PM. 2005. The teratology of autism. Int J Dev Neurosci. Apr-May;23(2-3):189-199. Review.

Rodier PM. 2004. Environmental causes of central nervous system maldevelopment. Pediatrics. Apr;113(4 Suppl):1076-1083.

Devlin B, Bennett P, Dawson G, Figlewicz DA, Grigorenko EL, McMahon W, Minshew N, Pauls D, Smith M, Spence MA, Rodier PM, Stodgell C, and Schellenberg GD. 2004. Alleles of a reelin CGG repeat do not convey liability to autism in a sample from the CPEA network. Am J Med Genet. Apr 1;126B(1):46-50.

Conciatori M, Stodgell CJ, Hyman SL, O’Bara M, Militerni R, Bravaccio C, Trillo S, Montecchi F, Schneider C, Melmed R, Elia M, Crawford L, Spence SJ, Muscarella L, Guarnieri V, D'Agruma L, Quattrone A, Zelante L, Rabinowitz D, Pascucci T, Puglisi-Allegra S, Reichelt KL, Rodier PM, Persico AM. 2004. Association between the HOXA1 A218G polymorphism and increased head circumference in patients with autism. Biol Psychiatry. Feb 15;55(4):413-419.

Rodier PM. 2004. Warkany Lecture: Autism as a birth defect. Birth Defects Res Part A Clin Mol Teratol. Jan;70(1):1-6. [No abstract]

Rodier PM. 2002. Converging evidence for brain stem injury in autism. Dev Psychopathol. Summer;14(3):537-557.

Hyman SL, Rodier PM, Davidson P. 2001. Pervasive Developmental Disorders in Young Children [Editorial] JAMA Jun 27;285(24):3141-3142.

Ingram, J.L., Stodgell, C.J., Hyman, S.L., Figlewicz, D.A., Weitkamp, L.R., and Rodier, P.M. 2000. Discovery of allelic variants of HOXA1 and HOXB1: genetic susceptibility to autism spectrum disorders. Teratology. Dec;62(6):393-405.

Ingram, J.L., Peckham, S.M., Tisdale, B., and Rodier, P.M. 2000. Prenatal exposure of rats to valproic acid reproduces the cerebellar anomalies associated with autism. Neurotoxicol. Teratol. 22(3):319-324.

Rodier, P.M. 2000. The early origins of autism. Scientific American. Feb;282(2):56-63. [No abstract]

Rodier, P. M., and Hyman, S. L. 1998. Early environmental factors in autism. Mental Retardation--Developmental Disabilities Res. Rev., 4: 121-128. [No abstract]

Rodier, P. M., Ingram, J. L., Tisdale, B. and Croog, V. J. 1997. Linking etiologies in humans and animal models: Studies of autism. Reprod. Toxicol. 11:417-422.

Rodier, P. M., Bryson, S. E. and Welsh, J. P. 1997. Minor malformations and physical measurements in autism: data from Nova Scotia. Teratology 55: 319-325.

Rodier, P. M. Ingram, J. L., Tisdale, B., Nelson, S. and Romano, J. 1996. Embryological origin for autism: Developmental anomalies of the cranial nerve motor nuclei. J. Comp. Neurol. 370:247-261.

Rodier, P. M. 1996. An animal model of autism based on developmental data. MRDD Res. Rev. 2: 249-256. [No abstract]