Publications by authors named "Ened Rodriguez-Urgelles"

Article Synopsis
  • The study investigates the role of specific striatal circuits in motor control and behavior in both healthy and Huntington's Disease (HD) mice, focusing on the direct and indirect pathways from the dorsolateral (DLS) and dorsomedial striatum (DMS).
  • Optogenetic stimulation of these pathways in wild type mice showed slight improvements in locomotion and motor learning but did not affect exploratory behavior.
  • In contrast, the same stimulation in HD mice did not produce any behavioral changes, suggesting that targeting cortico-striatal circuits may be a more effective approach for treating motor symptoms in HD rather than focusing solely on striatal output pathways.
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Background: Huntington's Disease (HD) is a disorder that affects body movements. Altered glutamatergic innervation of the striatum is a major hallmark of the disease. Approximately 30% of those glutamatergic inputs come from thalamic nuclei.

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Huntington's Disease (HD) is a devastating disorder characterized by a triad of motor, psychiatric and cognitive manifestations. Psychiatric and emotional symptoms appear at early stages of the disease which are consistently described by patients and caregivers among the most disabling. Here, we show for the first time that Foxp2 is strongly associated with some psychiatric-like disturbances in the R6/1 mouse model of HD.

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Glycogen synthase kinase 3β (GSK3β) is a core protein, with a relevant role in many neurodegenerative disorders including Alzheimer's disease. The enzyme has been largely studied as a potential therapeutic target for several neurological diseases. Unfortunately, preclinical and clinical studies with several GSK3β inhibitors have failed due to many reasons such as excessive toxicity or lack of effects in human subjects.

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Glycogen Synthase Kinase 3 (GSK3) is an essential protein, with a relevant role in many diseases such as diabetes, cancer and neurodegenerative disorders. Particularly, the isoform GSK3β is related to pathologies such as Alzheimer's disease (AD). This enzyme constitutes a very interesting target for the discovery and/or design of new therapeutic agents against AD due to its relation to the hyperphosphorylation of the microtubule-associated protein tau (MAPT), and therefore, its contribution to neurofibrillary tangles (NFT) formation.

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