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H. Brent Clark, M.D., Ph.D. Professor, Department of Laboratory Medicine & Pathology E-mail: clark002@umn.edu

Research Interests:

am interested in animal models of neuropathologic processes. In particular, I have been working with transgenic murine models of human inherited cerebellar ataxias. These mice, derived from transgenic experiments in the laboratories of Dr. Harry Orr, Dr. Laura Ranum and Dr. Michael Koob, involve the introduction of human mutations for several forms of spinal cerebellar ataxia into mice. The approach of my laboratory is primarily morphological, with emphasis on immunohistochemistry to elucidate the pathological anatomy. I also am interested in studying the neuropathology of the human ataxias, particularly the inherited forms.

Selected Publications:

Kendi AT, McKinney AM, Clark HB, Kieffer SA. A pediatric case of low-grade lymphomatoid granulomatosis presenting with a cerebellar mass. AJNR Am J Neuroradiol. 2007 Oct;28(9):1803-5.

Ryan LJ, Bowman R, Zantek ND, Sherr G, Maxwell R, Clark HB, Mair DC. Use of therapeutic plasma exchange in the management of acute hemorrhagic leukoencephalitis: a case report and review of the literature. Transfusion. 2007 Jun;47(6):981-6. Review.

Serra HG, Duvick L, Zu T, Carlson K, Stevens S, Jorgensen N, Lysholm A, Burright E, Zoghbi HY, Clark HB, Andresen JM, Orr HT. RORalpha-mediated Purkinje cell development determines disease severity in adult SCA1 mice. Cell. 2006 Nov 17;127(4):697-708.

He Y, Zu T, Benzow KA, Orr HT, Clark HB, Koob MD. Targeted deletion of a single Sca8 ataxia locus allele in mice causes abnormal gait, progressive loss of motor coordination, and Purkinje cell dendritic deficits. J Neurosci. 2006 Sep 27;26(39):9975-82.

Ikeda Y, Dick KA, Weatherspoon MR, Dalton JC, Stevanin G, Durr A, Zuhlke C, Burk K, Brice A, Clark HB, Schut LJ, Day JW, Ranum LPW: Spectrin mutations cause spinocerebellar ataxia type 5. Nature Genetics 38:184-190, 2006

Kordasiewicz HB, Thompson RM, Clark HB, and Gomez CM: C-termini of P/Q-type Ca2+ channel of alpha1A subunits translocate to nuclei and promote polyglutamine-mediated toxicity. Hum. Mol. Genetics 15: 1587-1599, 2006.

Moseley ML, Zu T, Ikeda Y, Gao W, Mosemiller AK, Daughters R, Chen
G, Weatherspoon MR, Clark HB, Ebner TJ, Day JW and Ranum LPW:
Bidirectional expression of CUG and CAG expansion transcripts and
intranuclear polyglutamine inclusions in spinocerebellar ataxia type
8. Nature Genetics, 38:758-769, 2006.