Neurobiology of disease
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Neurosteroids are involved in sex-specific epilepsies. Allopregnanolone and related endogenous neurosteroids in the brain control excessive neuronal excitability and seizure susceptibility. Neurosteroids activate GABA-A receptors, especially extrasynaptic αγδ-GABA-A receptor subtypes that mediate tonic inhibition and thus dampen network excitability. ⋯ Neurosteroids also regulate the plasticity of synaptic and extrasynaptic GABA-A receptors in the hippocampus and other regions involved in epilepsy pathology. Based on these studies, we proposed a neurosteroid replacement therapy for catamenial epilepsy. Thus, neurosteroids are novel drug targets for pharmacotherapy of epilepsy.
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Neurobiology of disease · Dec 2014
ReviewGender issues in the neurobiology of epilepsy: a clinical perspective.
A patient's hormonal milieu contributes to the timing of emergence of several epilepsy syndromes that are known to begin at puberty and recede with the end of reproductive potential. One's hormonal balance at any particular moment contributes to seizure occurrence in both men and women. ⋯ Seizures and “silent” epileptiform discharges in turn affect the hypothalamic pituitary axis and can cause release of hormones at inappropriate times leading to sexual dysfunction, menstrual irregularity, infertility and premature termination of reproductive states. Combined with psychological consequences of epilepsy, this sexual dysfunction has deleterious effects on the quality of life in patients and their partners.
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Neurobiology of disease · Dec 2014
ReviewSystem-based approaches to decode the molecular links in Parkinson's disease and diabetes.
A growing body of evidence indicates an increased risk for developing Parkinson's disease (PD) among people with type 2 diabetes (T2DM). The relationship between the etiology and development of both chronic diseases is beginning to be uncovered and recent studies show that PD and T2DM share remarkably similar dysregulated pathways. ⋯ Further, transcriptional signatures that modulate the neurodegenerative phenotype in T2DM have been identified. Here we contextualize the current experimental approaches to dissect the mechanisms underlying the association between PD and T2DM and discuss the existing challenges toward the understanding of the coexistence of these devastating aging diseases.