Journal ArticleDOI
Early synaptic pathophysiology in neurodegeneration: insights from Huntington's disease
TLDR
Investigations of synaptic transmission and plasticity in mouse models of Huntington's disease (HD) demonstrate neuronal dysfunction long before the onset of classical disease indicators, and recent human studies reveal synaptic dysfunction decades before predicted clinical diagnosis in HD gene carriers.About:
This article is published in Trends in Neurosciences.The article was published on 2010-11-01. It has received 279 citations till now. The article focuses on the topics: Huntington's disease & Neurodegeneration.read more
Citations
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Journal ArticleDOI
Harnessing neuroplasticity for clinical applications
Steven C. Cramer,Mriganka Sur,Bruce H. Dobkin,Charles J O'Brien,Terence D. Sanger,John Q. Trojanowski,Judith M. Rumsey,Ramona Hicks,Judy L. Cameron,Daofen Chen,Wen G. Chen,Leonardo G. Cohen,Christopher deCharms,Charles J. Duffy,Guinevere F. Eden,Eberhard E. Fetz,Rosemarie Filart,Michelle Freund,Steven J. Grant,Suzanne N. Haber,Peter W. Kalivas,Bryan Kolb,Arthur F. Kramer,Minda Lynch,Helen S. Mayberg,Patrick S. McQuillen,Ralph Nitkin,Alvaro Pascual-Leone,Patricia A. Reuter-Lorenz,Nicholas D. Schiff,Anu Sharma,Lana Shekim,Michael P. Stryker,Edith V. Sullivan,Sophia Vinogradov +34 more
TL;DR: Integration of information across disciplines should enhance opportunities for the translation of neuroplasticity and circuit retraining research into effective clinical therapies.
Journal ArticleDOI
BDNF-based synaptic repair as a disease-modifying strategy for neurodegenerative diseases
TL;DR: The key issues in translating BDNF biology into synaptic repair therapies are reviewed, which pave the way for a 'synaptic repair' therapy for neurodegenerative diseases that targets pathophysiology rather than pathogenesis.
Journal ArticleDOI
The "quad-partite" synapse: microglia-synapse interactions in the developing and mature CNS.
TL;DR: Current knowledge sheds new light on the critical functions of these mysterious cells in synapse development and function in the healthy CNS, but has also incited several new and interesting questions that remain to be explored.
Journal ArticleDOI
Huntington's disease: underlying molecular mechanisms and emerging concepts.
TL;DR: It is demonstrated that in addition to effects on folding, aggregation, and clearance pathways, a general transcriptional mechanism also dictates the expression of polyglutamine proteins.
Journal ArticleDOI
Pathophysiology of Huntington’s Disease: Time-Dependent Alterations in Synaptic and Receptor Function
Lynn A. Raymond,Véronique M. André,Carlos Cepeda,Clare M. Gladding,Austen J. Milnerwood,Michael Levine +5 more
TL;DR: The main findings indicate that HD treatments need to be designed according to the stage of disease progression and should consider regional differences, with a complex series of alterations that are region-specific and time-dependent.
References
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Journal ArticleDOI
A synaptic model of memory: long-term potentiation in the hippocampus
TL;DR: The best understood form of long-term potentiation is induced by the activation of the N-methyl-d-aspartate receptor complex, which allows electrical events at the postsynaptic membrane to be transduced into chemical signals which, in turn, are thought to activate both pre- and post Synaptic mechanisms to generate a persistent increase in synaptic strength.
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LTP and LTD: an embarrassment of riches.
Robert C. Malenka,Mark F. Bear +1 more
TL;DR: This work reviews those forms of LTP and LTD for which mechanisms have been most firmly established and examples are provided that show how these mechanisms can contribute to experience-dependent modifications of brain function.
Journal ArticleDOI
Huntington's disease.
TL;DR: Effective intervention by clinicians is possible in terms of providing patients and families with accurate information about the disease, counseling them about availability of genetic testing at specialized centers, and in giving them sound advice regarding work, driving, relationships, finances, research participation, and support groups.
Journal ArticleDOI
Inclusion body formation reduces levels of mutant huntingtin and the risk of neuronal death
TL;DR: It is shown, by survival analysis, that neurons die in a time-independent fashion but one that is dependent on mutant huntingtin dose and polyglutamine expansion; many neurons die without forming an inclusion body.
Journal ArticleDOI
Extrasynaptic NMDARs oppose synaptic NMDARs by triggering CREB shut-off and cell death pathways
TL;DR: It is reported that synaptic and extrasynaptic NMDA (N-methyl-D-aspartate) receptors have opposite effects on CREB (cAMP response element binding protein) function, gene regulation and neuron survival.
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