Browsing by Author "Rangel, R."
Now showing 1 - 2 of 2
Results Per Page
Sort Options
- Expression of adenosine kinase in human mesial temporal lobe epilepsy with hippocampal sclerosis: A preliminary studyPublication . Leal, B.; Rangel, R.; Chaves, J.; Carvalho, C.; Bettencourt, A.; Zenatti, L.; Santos, A.; Magalhães, T.; Martins da Silva, A.; Correia de Sá, P.; Martins da Silva, B.; Costa, P.P.Background: Adenosine is a ubiquitous homeostatic molecule that acts as an “endogenous neuromodulator”. Adenosine attenuates neuronal activity either presynaptically by inhibiting neurotransmitter release or by controlling neurotransmitter responsiveness at post-synaptic sites. Unbalanced adenosine metabolism has been implicated in pathological conditions such as epilepsy. Adenosine kinase (ADK), synthetized by astrocytes, is the key regulator of extracellular adenosine levels in the brain. Evidences from experimental studies support a role for ADK in brain injury associated with astrogliosis, a morphological hallmark of Mesial Temporal Lobe Epilepsy with Hippocampal Sclerosis (MTLE-HS). In fact, expression of astrocytic ADK was found to be increased in the hippocampus and temporal cortex of MTLE-HS patients. Overexpression of ADK decreases extracellular adenosine and consequently may cause seizures. The aim of this study was to characterize ADK gene expression in MTLE-HS patients. Methods: Previous studies used immunohistochemistry and Western blot analysis to investigate ADK expression. Here we quantified the expression levels of ADK by Real-Time PCR in the hippocampus (lesional and peri-lesional cortical area) of 10 MTLE-HS patients submitted to surgery as compared with 9 autopsy controls with no history of neurological disorders. Results: Our results showed that ADK expression levels were similar in the hippocampus and temporal cortex of MTLE-HS patients when compared to healthy controls. Conclusion: Our preliminary data demonstrate that ADK expression levels are not altered in MTLE-HS. These results do not preclude post-transcriptional ADK abnormalities at both protein and functional levels. Our results should be confirmed in a larger cohort as well as with complementary methodologies.
- Human herpes virus 6B and mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE-HS): is there a link?Publication . Leal, B.; Castelo Branco, R.; Rangel, R.; Chaves, J.; Carvalho, C.; Bettencourt, A.; Honavar, M.; Melo Pires, M.; Santos, A.; Magalhães, T.; Lopes, J.; Ramalheira, J.; Martins da Silva, A.; Costa, P.P.; Martins da Silva, B.Purpose: Human Herpesvirus 6 (HHV-6) is a ubiquitous virus acquired mainly during the first 2 years of life. Mesial Temporal Lobe Epilepsy with Hippocampal Sclerosis (MTLE-HS) is the most frequent pharmacoresistant epilepsy. One of the most common antecedents of MTLE-HS is febrile seizures (FS). Although the aetiology of MTLE-HS remains unclear, evidences suggest that HHV-6 infection could be implicated. The objective of this study was to investigate the presence of HHV-6B DNA in the hippocampus and adjoining temporal cortex of MTLE-HS patients submitted to surgery. Methods: A total of 22 MTLE-HS (13 females and nine males) cases were studied. The mean age at surgery was 39 9 years and mean age at onset of seizures was 10 6 years. These study cohort was compared to a group of 10 epileptic patients without MTLE-HS (six females, four males; mean age = 26 15 years) and with autopsy material from nine individuals without neurological disease. HHV-6B DNA was identified by real-time PCR with specific TaqMan probes. Results: We detected HHV-6B DNA in only one hippocampus from a MTLE-HS patient. This patient had a disease duration of 36 years and a history of febrile seizures in childhood. None of the non-MTLE or controls specimens showed positivity for HHV-6B. Conclusions: Our findings do not support a relevant etiologic role for HHV-6B in MTLE-HS, at least in this population. However, the possible role of viral infection in MTLE-HS epileptogenic process, in individual cases, cannot be excluded.