Navigation überspringen
Universitätsbibliothek Heidelberg
Status: Bibliographieeintrag

Verfügbarkeit
Standort: ---
Exemplare: ---
heiBIB
Verfasst von:Bading, Hilmar [VerfasserIn]   i
Titel:Therapeutic targeting of the pathological triad of extrasynaptic NMDA receptor signaling in neurodegenerations
Verf.angabe:Hilmar Bading
Umfang:10 S.
Fussnoten:Published February 16, 2017 ; Published online: 16 February, 2017 ; Gesehen am 27.06.2018
Titel Quelle:Enthalten in: Journal of experimental medicine
Jahr Quelle:2017
Band/Heft Quelle:214(2017), 3, S. 569-578
ISSN Quelle:1540-9538
Abstract:Activation of extrasynaptic N-methyl-d-aspartate (NMDA) receptors causes neurodegeneration and cell death. The disease mechanism involves a pathological triad consisting of mitochondrial dysfunction, loss of integrity of neuronal structures and connectivity, and disruption of excitation-transcription coupling caused by CREB (cyclic adenosine monophosphate-responsive element-binding protein) shut-off and nuclear accumulation of class IIa histone deacetylases. Interdependency within the triad fuels an accelerating disease progression that culminates in failure of mitochondrial energy production and cell loss. Both acute and slowly progressive neurodegenerative conditions, including stroke, Alzheimer’s disease, amyotrophic lateral sclerosis, and Huntington’s disease, share increased death signaling by extrasynaptic NMDA receptors caused by elevated extracellular glutamate concentrations or relocalization of NMDA receptors to extrasynaptic sites. Six areas of therapeutic objectives are defined, based on which a broadly applicable combination therapy is proposed to combat the pathological triad of extrasynaptic NMDA receptor signaling that is common to many neurodegenerative diseases.
DOI:doi:10.1084/jem.20161673
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Verlag: http://dx.doi.org/10.1084/jem.20161673
 Verlag: http://jem.rupress.org/content/214/3/569
 DOI: https://doi.org/10.1084/jem.20161673
Sprache:eng
K10plus-PPN:157690315X
Verknüpfungen:→ Zeitschrift

Permanenter Link auf diesen Titel (bookmarkfähig):  https://katalog.ub.uni-heidelberg.de/titel/68274786   QR-Code
zum Seitenanfang