DYNLT1 gene expression is downregulated in whole blood of patients at different Huntington's disease stages.

Huntington's disease (HD) is a neurodegenerative disorder caused by a CAG nucleotide expansion, which encodes the amino acid glutamine, in the huntingtin gene. HD is characterized by motor, cognitive, and psychiatric dysfunctions. In a previous study, we showed by qPCR that some genes altered in an HD mouse model were also altered in blood of HD patients. These alterations were mainly with respect to the dynein family. Therefore, this study aimed to investigate whether dynein light chain Tctex type 1 (DYNLT1) is altered in HD patients and if there is a correlation between DYNLT1 gene expression changes and disease progression. We assessed the DYNLT1 gene expression in the blood of 19 HD patients and 20 healthy age-matched controls. Also, in 6 of these patients, we analyzed the DYNLT1 expression at two time points, 3 years apart. The DYNLT1 gene expression in the whole blood of HD patients was significantly downregulated and this difference was widened in later stages. These data suggest that DYNLT1 could emerge as a peripheral prognostic indicator in HD and, also, might be a target for potential intervention in the future.

The cannabinoid agonist WIN-2 affects acquisition but not consolidation of a spatial information in training and retraining processes: Relation with transcriptional regulation of the endocannabinoid system?

The endocannabinoid system is capable of modulating multiple physiological brain functions including learning and memory. Moreover, there is evidence that the processes of acquisition and consolidation have distinct biological basis. We used the cannabinoid agonist WIN 55,212-2 (WIN-2) to investigate whether chronic CB1 activation affects acquisition and consolidation differently by evaluating gene expression in the hippocampus (HIP) and prefrontal cortex (PFC). Swiss mice were treated with WIN-2 (2 mg/kg) and submitted to the Morris water maze to evaluate different aspects of memory. We observed short-term memory impairment in acquisition of the spatial task while consolidation remained unchanged. In the PFC, animals that received WIN-2 prior to the task exhibited increased expression of the 2-AG synthesis enzyme diacylglycerol lipase and decreased levels of the degradation enzyme monoacylglycerol lipase, while mice that were treated after the task for the evaluation of consolidation exhibited the opposite profile. With respect to genes related to AEA metabolism, no correlation between the molecular and behavioral data could be established. In this sense, the cognitive impairment in the acquisition promoted by WIN-2 treatment may be related to a possible increase in the concentration of 2-AG in the PFC. Overall, this study confirms the relevance of the endocannabinoid system in the modulation of cognitive processes. A better understanding of the mechanisms underlying endocannabinoids roles in cognition could provide guidance for the development of treatments to reduce the cognitive deficits caused by drug abuse.

Albendazole therapy for giant subarachnoid cysticerci.

Albendazole is considered to be the drug of choice for treatment of parenchymal brain cysticercosis. Its efficacy, however, for treatment of subarachnoid cysticerci has not been established, to our knowledge. In this study, we treated four patients who had giant subarachnoid cysticerci with albendazole at daily doses of 15 mg/kg of body weight for 8 days. Computed tomographic studies showed that all cysts disappeared 3 months after the end of treatment. This was associated with marked clinical improvement in every case. Our results indicated that albendazole is highly effective for treatment of this form of the disease.

Epilepsy due to neurocysticercosis: analysis of 203 patients.

We reviewed clinical, EEG, and CT findings of 203 patients with epilepsy due to neurocysticercosis. Seizures were generalized in 121 patients and partial in 82. Thirty-two patients had focal signs and eight had papilledema. Eighty-one had generalized and 16 had focal EEG abnormalities. CT showed parenchymal brain calcifications in 53 patients and cysts in 150. There was an increased rate of focal signs in patients with single cysts as compared with patients with multiple cysts, and focal EEG abnormalities were present only in patients with single cysts. Fifty patients were lost to follow-up. The remaining 153 patients were followed for 28 +/- 6 months; of these, 31 had calcifications and 122 had cysts. Anticonvulsants were started after the first visit in every patient. The 31 patients with calcifications remained free of seizures. Ninety-five of the 122 patients with cysts were also treated with anticysticercal drugs; of these, 79 (83%) had control of seizures. In contrast, only seven (26%) of 27 patients who did not receive anticysticercal drugs had control of seizures, indicating a strong correlation between the use of anticysticercal drugs and seizure control. Finally, of the 21 patients in whom anticonvulsants were withdrawn, 16 had relapses.

Bilateral internuclear ophthalmoplegia after smoking "crack" cocaine.

A previously healthy 35-year-old man developed sudden diplopia after smoking "crack" cocaine. Neuroophthalmologic examination revealed findings consistent with a tegmental mesencephalic lesion which correlated closely with the computed tomographic documentation of a small midbrain hemorrhage. Cocaine abuse is a recognized cause of intracranial hemorrhage. In most patients, however, the bleeding is localized in the subarachnoid space or the subcortical white matter. To our knowledge, this is the first case of isolated midbrain hemorrhage secondary to cocaine abuse.