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Differential alterations of neocortical GluN receptor subunits in patients with mixed subcortical ischemic vascular dementia and Alzheimer's disease.

Authors: Mohamed, Nur-Ezan  Lee, Jasinda H  Francis, Paul T  Esiri, Margaret M  Chen, Christopher P  Lai, Mitchell K P 
Citation: Mohamed NE, etal., J Alzheimers Dis. 2015;44(2):431-7. doi: 10.3233/JAD-141764.
Pubmed: (View Article at PubMed) PMID:25261450
DOI: Full-text: DOI:10.3233/JAD-141764


BACKGROUND: Glutamatergic deficits are well-established neurochemical findings in Alzheimer's disease (AD) and are thought to underlie both cognitive and behavioral symptoms of the disease. However, it is unclear whether subcortical ischemic vascular dementia (SIVD) and mixed SIVD/AD (MixD) manifest similar changes in the glutamatergic system.
OBJECTIVE: To measure the immunoreactivities of NMDA receptor GluN1, GluN2A, and GluN2B subunits in SIVD and MixD.
METHODS: Postmortem neocortical tissues from a cohort of well-characterized, longitudinally followed-up patients with SIVD and MixD, together with age-matched controls, were processed for immunoblotting with GluN subunit-specific antibodies.
RESULTS: There was a significant reduction of GluN1 only in MixD, while significant increases of GluN2A and GluN2B were found only in SIVD. Furthermore, GluN1 loss and GluN2A/2B upregulation was associated respectively with higher Braak stages and lacunar infarct scores.
CONCLUSIONS: Our data suggest that the differential alterations of GluN subunits in SIVD and MixD may result from separate, interacting disease processes, and point to the potential utility of glutamatergic approaches for pharmacotherapy.

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CRRD Object Information
CRRD ID: 13792687
Created: 2018-09-20
Species: All species
Last Modified: 2018-09-20
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.