Please use this identifier to cite or link to this item: https://doi.org/10.3233/JAD-2010-1398
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dc.titleAltered NCAM Expression Associated with the Cholinergic System in Alzheimer's Disease
dc.contributor.authorAisa, Barbara
dc.contributor.authorGil-Bea, Francisco J
dc.contributor.authorSolas, Maite
dc.contributor.authorGarcia-Alloza, Monica
dc.contributor.authorChen, Christopher P
dc.contributor.authorLai, Mitchell K
dc.contributor.authorFrancis, Paul T
dc.contributor.authorJavier Ramirez, Maria
dc.date.accessioned2021-04-06T02:45:50Z
dc.date.available2021-04-06T02:45:50Z
dc.date.issued2010-01-01
dc.identifier.citationAisa, Barbara, Gil-Bea, Francisco J, Solas, Maite, Garcia-Alloza, Monica, Chen, Christopher P, Lai, Mitchell K, Francis, Paul T, Javier Ramirez, Maria (2010-01-01). Altered NCAM Expression Associated with the Cholinergic System in Alzheimer's Disease. JOURNAL OF ALZHEIMERS DISEASE 20 (2) : 659-668. ScholarBank@NUS Repository. https://doi.org/10.3233/JAD-2010-1398
dc.identifier.issn13872877
dc.identifier.issn18758908
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/188383
dc.description.abstractNeurotransmitter system dysfunction and synapse loss have been recognized as hallmarks of Alzheimer's disease (AD). Our hypothesis is that specific neurochemical populations of neurons might be more vulnerable to degeneration in AD due to particular deficits in synaptic plasticity. We have studied, in postmortem brain tissue, the relationship between levels of synaptic markers (NCAM and BDNF), neurochemical measurements (cholinacetyltransferase activity, serotonin, dopamine, GABA, and glutamate levels), and clinical data (cognitive status measured as MMSE score). NCAM levels in frontal and temporal cortex from AD patients were significantly lower than control patients. Interestingly, these reductions in NCAM levels were associated to an ApoE4 genotype. Levels of BDNF were also significantly reduced in both frontal and temporal regions in AD patients. The ratio between plasticity markers and neurochemical measurements was used to study which of the neurochemical populations was particularly associated to plasticity changes. In both the frontal and temporal cortex, there was a significant reduction in the ChAT/NCAM ratio in AD samples compared to controls. None of the ratios to BDNF were different between control and AD samples. Furthermore, Pearson's product moment showed a significant positive correlation between MMSE score and the ChAT/NCAM ratio in frontal cortex (n=19; r=0.526*; p=0.037) as well as in temporal cortex (n=19; r=0.601*; p=0.018) in AD patients. Altogether, these data suggest a potential involvement of NCAM expressing neurons in the cognitive deficits in AD. © 2010 - IOS Press and the authors. All rights reserved.
dc.language.isoen
dc.publisherIOS PRESS
dc.sourceElements
dc.subjectScience & Technology
dc.subjectLife Sciences & Biomedicine
dc.subjectNeurosciences
dc.subjectNeurosciences & Neurology
dc.subjectBDNF
dc.subjectChAT
dc.subjectcognitive deficits
dc.subjectfrontal cortex (BA10)
dc.subjectMMSE
dc.subjectplasticity
dc.subjecttemporal cortex (BA20)
dc.subjectCELL-ADHESION MOLECULE
dc.subjectNEUROTROPHIC-FACTOR
dc.subjectHIPPOCAMPAL PLASTICITY
dc.subjectSYNAPTIC PLASTICITY
dc.subjectAPOLIPOPROTEIN-E
dc.subjectMESSENGER-RNA
dc.subjectUP-REGULATION
dc.subjectHUMAN BRAIN
dc.subjectLONG-TERM
dc.subjectDEFICITS
dc.typeArticle
dc.date.updated2021-04-03T05:16:29Z
dc.contributor.departmentDEPT OF PHARMACOLOGY
dc.description.doi10.3233/JAD-2010-1398
dc.description.sourcetitleJOURNAL OF ALZHEIMERS DISEASE
dc.description.volume20
dc.description.issue2
dc.description.page659-668
dc.description.placeNETHERLANDS
dc.published.statePublished
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