Huntington's disease: easing the NMDAR traffic jam

Daggett, Anthony; Xu, Yang

doi:10.1038/nm.3283

Cited by 2 publications

(2 citation statements)

References 12 publications

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“…Administration of ephrin-B2 counteracts this loss of extrasynaptic and synaptic NMDAR both in vitro and in vivo in the NMDAR-antibody transfer mouse model ( Mikasova et al , 2012 ; Planagumà et al , 2016 ). Notably, aberrant NMDAR trafficking is also pivotal in the pathophysiology of Huntington’s disease ( Daggett and Yang, 2013 ), and reagents that regulate human ephrin-like receptors are under investigation for treatment of Huntington’s disease ( Ramakrishnan, 2003 ). Clinical practice offers another paradigm of a similar treatment approach in genetic and autoimmune neurology where 4-aminopyridine has proved beneficial in two disorders affecting P/Q type voltage-dependent calcium channels: episodic ataxia type 2 due to P/Q calcium channel gene mutations and Lambert-Eaton syndrome due to P/Q calcium channel autoantibodies ( Strupp et al , 2011 ).…”

Section: Conclusion and Future Directivesmentioning

confidence: 99%

Movement disorders with neuronal antibodies: syndromic approach, genetic parallels and pathophysiology

Balint

Vincent

Meinck

et al. 2017

Brain

148

155

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Section: Conclusion and Future Directivesmentioning

confidence: 99%

Movement disorders with neuronal antibodies: syndromic approach, genetic parallels and pathophysiology

Balint

Vincent

Meinck

et al. 2017

Brain

148

155

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“…Furthermore, previous studies have indicated that NMDA receptors were involved in the pathological mechanisms of Parkinson, Alzheimer and Huntington diseases (Xu et al . ; Daggett & Yang ; Hanson et al . ).…”

Section: Discussionmentioning

confidence: 99%

Transcriptome comparison in the pituitary–adrenal axis between Beagle and Chinese Field dogs after chronic stress exposure

Luo

Fang

et al. 2015

Animal Genetics

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Chronic stress can induce a series of maladjustments, and the response to stress is partly regulated by the hypothalamus-pituitary-adrenal axis. The aim of this study was to investigate the genetic mechanisms of this axis regulating stress responsiveness. The pituitary and adrenal cortex of Beagle and Chinese Field Dog (CFD) from a stress exposure group [including Beagle pituitary 1 (BP1), CFD pituitary 1 (CFDP1), Beagle adrenal cortex 1 (BAC1), CFD adrenal cortex 1 (CFDAC1)] and a control group [including Beagle pituitary 2 (BP2), CFD pituitary 2 (CFDP2), Beagle adrenal cortex 2 (BAC2), CFD adrenal cortex 2 (CFDAC2)], selected to perform RNA-seq transcriptome comparisons, showed that 40, 346, 376, 69, 70, 38, 57 and 71 differentially expressed genes were detected in BP1 vs. BP2, CFDP1 vs. CFDP2, BP1 vs. CFDP1, BP2 vs. CFDP2, BAC1 vs. BAC2, CFDAC1 vs. CFDAC2, BAC1 vs. CFDAC1 and BAC2 vs. CFDAC2 respectively. NPB was a gene common to BAC1 vs. BAC2 and CFDAC1 vs. CFDAC2, indicating it was a potential gene affecting response to chronic stress, regardless of the extent of chronic stress induced. PLP1 was a gene common to BP1 vs. CFDP1 and BP2 vs. CFDP2, suggesting its important roles in affecting the stress-tolerance difference between the two breeds, regardless of whether there was stress exposure or not. Pathway analysis found 12, 4, 11 and 1 enriched pathway in the comparisons of BP1 vs. CFDP1, BP2 vs. CFDP2, CFDP1 vs. CFDP2 and BAC1 vs. BAC2 respectively. Glutamatergic synapse, neuroactive ligand-receptor interaction, retrograde endocannabinoid signaling, GABAergic synapse, calcium signaling pathway and dopaminergic synapse were the most significantly enriched pathways in both CFDP1 vs. CFDP2 and BP1 vs. CFDP1. GO, KEGG pathway and gene network analysis demonstrated that GRIA3, GRIN2A, GRIN2B and NPY were important in regulating the stress response in CFD. Nevertheless, ADORA1, CAMK2A, GRM1, GRM7 and NR4A1 might be critical genes contributing to the stress-tolerance difference between CFD and Beagle when subjected to stress exposure. In addition, RGS4 and SYN1 might play important roles both in regulating the stress response in CFD and in affecting the stress-tolerance difference in different breeds. These observations clearly showed that some genes in the adrenal cortex and pituitary could regulate the stress response in Beagle and CFDs, whereas some others could affect the stress-tolerance difference between these two breeds. Our results can contribute to a more comprehensive understanding of the genetic mechanisms of response to chronic stress.

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Huntington's disease: easing the NMDAR traffic jam

Cited by 2 publications

References 12 publications

Movement disorders with neuronal antibodies: syndromic approach, genetic parallels and pathophysiology

Movement disorders with neuronal antibodies: syndromic approach, genetic parallels and pathophysiology

Transcriptome comparison in the pituitary–adrenal axis between Beagle and Chinese Field dogs after chronic stress exposure

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