"Neuronal loss and reactive glial proliferation induced by iron"
Nitric oxide synthase and NMDA receptor expressions in cavernoma
tissues with epileptogenesis
Authors: Kamida, T.; Takeda, Y.; Fujiki, M.; Abe, T.; Abe, E.;
Kobayashi, H.
Source: Acta Neurologica Scandinavica, Volume 116, Number 6, December
2007 , pp. 368-373(6)
Abstract:
Kamida T, Takeda Y, Fujiki M, Abe T, Abe E, Kobayashi H. Nitric oxide
synthase and NMDA receptor expressions in cavernoma tissues with
epileptogenesis.
Acta Neurol Scand 2007: 116: 368-373.
© 2007 The Authors Journal compilation © 2007 Blackwell Munksgaard.
Objectives -
To investigate the contribution of nitric oxide (NO) and the glutamate
systems to epileptogenicity of cavernoma (CA). Methods -
Using immunohistochemistry we examined NO synthases (NOS; neuronal,
inducible and endothelial) and N-methyl-D-aspartate (NMDA) receptor
subunits 1(NR1) and 2A/B (NR2A/B) in tissues, with and without
hemosiderin deposits, adjacent to CA resected from temporal (seven
patients) and frontal (one patient) lobes. Results -
All isoforms of NOS, especially iNOS expression, was significantly
upregulated in company with NR2A/B expression, not only in declining
neuronal cells but also in reactive astrocytes in the tissue, with
hemosiderin deposits, adjacent to CA and moreover the degree of iNOS
expression was significantly correlated with seizure frequency.
Conclusions -
These preliminary results sustain a speculation that excessive NO may
generate in the tissue surrounding CA with repeated microhaemorrhaging
and seizures. The neuronal loss and reactive glial proliferation
induced by iron or NO may play a role in epileptogenesis.
Keywords: nitric oxide synthase; N-methyl-D-aspartate; cavernoma;
hemosiderin deposits; epileptogenesis
Document Type: Research article
DOI: 10.1111/j.1600-0404.2007.00885.x
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ironjustice@aol.com - 14 Nov 2007 07:58 GMT
>> On Nov 10, 3:15 am, "ironjust...@aol.com" <ironjust...@aol.com> wrote:The neuronal loss and reactive glial proliferation
induced by iron or NO may play a role in epileptogenesis.<<
"iron overload other than the C282Y mutation underlies epilepsy"
J Neurol Neurosurg Psychiatry 2001;70:551-553 ( April )
Short report
Iron overload without the C282Y mutation in patients with epilepsy
M Ikeda
Department of Clinical Research, National Saigata Hospital, Ohgata-
machi, Niigata 949-3193, Japan massie@saigata-nh.go.jp
Received 7 September 2000 and in revised form 13 December 2000;
Accepted 14 December 2000
To test the hypothesis that iron overload predisposes to epilepsy,
transferrin saturation in 130 patients with epilepsy and sex and age
matched 128 control subjects without epilepsy were studied. Mean
transferrin saturation was significantly higher in the epilepsy group
(39.9 (SD 19.6)%) than in the control group (29.1 (SD 14.9)%).
Abnormally high transferrin saturations (men>60%, women>48%) were
found in 10 patients with epilepsy but in only one subject without
epilepsy. Antiepileptic drugs did not affect the transferrin
saturation. Of the 11 with abnormally high transferrin saturation, two
with epilepsy were heterozygotic for H63D in the haemochromatosis gene
but no patient had the C282Y mutation. These results indicate that
iron overload other than the C282Y mutation underlies epilepsy.
Keywords: epilepsy; haemochromatosis; iron overload
--------------------------------------------------------------------------------
© 2001 by Journal of Neurology, Neurosurgery, and Psychiatry
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> "Neuronal loss and reactive glial proliferation induced byiron"
>
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>
> DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk