Publications by authors named "Veronica Noches"

Article Synopsis
  • The text discusses amyotrophic lateral sclerosis (ALS), highlighting the degeneration of motor neurons and the formation of protein aggregates, particularly those involving RNA-binding proteins like TDP-43 and FUS/TLS.
  • It explains that these aggregates result from a process called liquid-to-solid phase separation, which is linked to changes in mRNA expression and protein levels.
  • The review emphasizes the significance of epigenetic factors, such as DNA methylation and histone modifications, in understanding ALS and suggests that targeting these mechanisms may lead to promising therapies.
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Article Synopsis
  • TDP-43 aggregation is linked to neurodegenerative diseases like ALS and FTD, making it a target for therapeutic approaches.* -
  • Researchers discovered that the N-terminal fragment of RGNEF (NF242) can bind to TDP-43, preventing its interaction with RNA, which is crucial for its pathogenic role.* -
  • Experiments in fruit flies and mice show that NF242 can improve symptoms and delay neurodegeneration associated with TDP-43, indicating potential as a treatment for related disorders.*
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RCOR1 is a known transcription repressor that recruits and positions LSD1 and HDAC1/2 on chromatin to erase histone methylation and acetylation. However, there is currently an incomplete understanding of RCOR1's range of localization and function. Here, we probe RCOR1's distribution on a genome-wide scale and unexpectedly find that RCOR1 is predominantly associated with transcriptionally active genes.

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Epilepsy is a neurological disorder of genetic or environmental origin characterized by recurrent spontaneous seizures. A rodent model of temporal lobe epilepsy is induced by a single administration of pilocarpine, a non-selective cholinergic muscarinic receptor agonist. The molecular changes associated with pilocarpine-induced seizures are still poorly described.

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Background: Basolateral amygdalar projections to the prefrontal cortex play a key role in modulating behavioral responses to stress stimuli. Among the different neuromodulators known to impact basolateral amygdalar-prefrontal cortex transmission, the corticotrophin releasing factor (CRF) is of particular interest because of its role in modulating anxiety and stress-associated behaviors. While CRF type 1 receptor (CRFR1) has been involved in prefrontal cortex functioning, the participation of CRF type 2 receptor (CRFR2) in basolateral amygdalar-prefrontal cortex synaptic transmission remains unclear.

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Background: Increased locomotor activity in response to the same stimulus is an index of behavioral sensitization observed in preclinical models of drug addiction and compulsive behaviors. Repeated administration of quinpirole, a D2/D3 dopamine agonist, induces locomotor sensitization. This effect is potentiated and accelerated by co-administration of U69593, a kappa opioid receptor agonist.

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There is significant functional evidence showing that corticotropin-releasing factor type-2 receptor (CRF2R) and corticotropin-releasing factor-binding protein (CRF-BP) regulate glutamatergic synapses onto ventral tegmental area (VTA) dopaminergic neurons. It has been shown that CRF requires CRF-BP to potentiate N-methyl-D-aspartate receptors in dopaminergic neurons through CRF2R, and that increases glutamate release in cocaine-treated rats through the activation of CRF2R only by agonists with high affinity to CRF-BP. Furthermore, this CRF-mediated increase in VTA glutamate is responsible for stress-induced relapse to cocaine-seeking behaviour.

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Background: Adult hypothyroidism is a highly prevalent condition that impairs processes, such as learning and memory. Even though tetra-iodothyronine (T(4)) treatment can overcome the hypothyroidism in the majority of cases, it cannot fully recover the patient's learning capacity and memory. In this work, we analyzed the cellular and molecular changes in the adult brain occurring with the development of experimental hypothyroidism.

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The transcription factor Nur77 has been identified as a neuronal activation marker of stressful stimuli in the central nervous system. Nur77 plays a key role at all levels of the hypothalamus-pituitary-adrenal axis during the stress response. However, the participation of Nur77 in extra-hypothalamic responses to stress is unknown.

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