[Abstract Title]. - Society for Neuroscience

Disclosures: Y. Hsieh , None; R. Miller, None; C. Wilson, None.
Poster
251. Demyelinating Disorders: Animal Models and Human Studies I
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 251.30/W23
Topic: C.08.b. Animal models
Support: FSS, Denmark
Title: Demyelination in experimental cerebral malaria
Authors: *C. HEMPEL 1,2,4 , L. WIESE 5,4,3 , J. KURTZHALS 4,2 , M. PENKOWA 3 ;
1 Univ. Copehagen, Cophenhagen, Denmark; 2 Ctr. for Med. Parasitology, 3 Section of
Neuroprotection, Univ. of Copenhagen, Copenhagen, Denmark; 4 Dept. of Clin. Microbiology,
Copenhagen Univ. Hosp., Copenhagen, Denmark; 5 Dept. of Infectious Dis., Hvidovre Hosp.,
Hvidovre, Denmark
Abstract: Cerebral malaria (CM) is a serious and often fatal complication of Plasmodium
falciparum malaria. It is an acute encephalopathy with loss of consciousness, convulsions and
fever. The underlying pathology includes dysregulated cytokine expression, increased
permeability of the blood-brain barrier and sequestration of host cells. Neurological sequelae are
common in survivors but no pathological processes responsible for the sequelae have been
identified. Since the neurological sequelae are often reversible, we hypothesised that
demyelination, followed by remyelination, could be involved.
We used the murine CM model (P. berghei infection in C57BL/6 mice) to study the possibility
that CM results in demyelination. Experimental murine and human CM share several clinical and
pathological characteristics. Brains were perfusion fixed with Zamboni‟s fixative and embedded
in paraffin. Myelin was visualised immunohistochemically with antibodies specific for myelin
basic protein. Apoptosis was visualised with antibodies specific for caspase-3.
Extensive demyelination was detected in terminally ill mice. Demyelination was particularly
evident in the cerebellum and in the corpus callosum. Apoptosis was present in infected mice but
the number of caspase-postitive cells was not statistical different from uninfected mice. The
underlying mechanisms remain to be elucidated as well as the extent of remyelination and
neuronal damage.
Disclosures: C. Hempel, None; L. Wiese, None; J. Kurtzhals, None; M. Penkowa, None.