Publication Detail
The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
Neuron-specific age-related decreases in dopamine receptor subtype mRNAs.
Scott E Hemby; John Q Trojanowski; Stephen D Ginsberg (Profiled Author: Trojanowski, John Q)
Department of Pharmacology and Psychiatry/Behavioral Sciences, Yerkes National Primate Research Center, Neuroscience Division, Emory University School of Medicine, Atlanta, Georgia 30329, USA. shemby@pharm.emory.edu
The Journal of comparative neurology 2003;456(2):176-83.
Age-related decline in dopamine receptor levels has been observed in regional studies of animal and human brains; however, identifying specific cellular substrates and/or alterations in distinct neuronal populations remains elusive. To evaluate whether age-related decreases in dopamine receptor subtypes are associated with specific cell populations in the hippocampus and entorhinal cortex, antisense RNA amplification was combined with cDNA array analysis to examine effects of aging on D1-D5 dopamine receptor mRNA expression levels in hippocampal CA1 pyramidal neurons and entorhinal cortex layer II stellate cells from post-mortem human brains (19-92 years). In CA1 pyramidal neurons, significant age-related decline was observed for dopamine receptor mRNAs (D1-D4, P < 0.001; D5, P < 0.05) but not for the cytoskeletal elements beta-actin, three-repeat (3R) tau, and four-repeat (4R) tau. In contrast, no significant changes were observed in stellate cells across the same cohort. Thus, senescence may be a factor responsible for cell-specific decrements in dopamine receptor gene expression in one population of neurons within a circuit that is critical for learning and memory. Furthermore, these results support the hypothesis that alterations in dopaminergic function may also be related to behavioral abnormalities, such as psychosis, that occur with aging.
3 Originating Grant
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1.
TROJANOWSKI, JOHN Q.
Alzheimer's Disease Core Center
15 July 1997 - 30 June 2016
NATIONAL INSTITUTE ON AGING
Total Funding: $ 25,158,594
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2.
Trojanowski, John Q
Molecular substrates of aging and neuron death
15 May 1997 - 30 April 2010
NATIONAL INSTITUTE ON AGING
Total Funding: $ 24,601,856
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3.
MUFSON, ELLIOTT JAY
Galanin in Alzheimer's Disease
29 September 1991 - 31 May 2012
NATIONAL INSTITUTE ON AGING
Total Funding: $ 5,750,823
Scientific Context
This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts and related grants with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.
Related Grants
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1.
Minoshima, Satoshi
In vivo mapping of gray matter loss in preclinical AD
30 September 2003 - 30 June 2009
NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE
Total Funding: $ 1,773,132
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2.
COTMAN, CARL W
MECHANISMS AND MOLECULAR PROFILES OF DEGENERATION IN AD
25 May 1995 - 30 April 2001
NATIONAL INSTITUTE ON AGING
Total Funding: $ 1,154,804
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3.
HYMAN, BRADLEY T
A Model of Early Alzheimer Disease
1 April 2011 - 31 March 2013
NATIONAL INSTITUTE ON AGING
Total Funding: $ 392,821
Related Publications
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1.
2010Ismael Santa-Maria; Jesus Avila; Alberto Rabano
Neuroscience letters 2010;468(3):225-8. -
2.
2004Stephen D Ginsberg; Irina Elarova; Marc Ruben; Fengzhu Tan; Scott E Counts; James H Eberwine; John Q Trojanowski; Scott E Hemby; Elliott J Mufson; Shaoli Che
Neurochemical research 2004;29(6):1053-64. -
3.
1998J A Court; S Lloyd; N Thomas; M A Piggott; E F Marshall; C M Morris; H Lamb; R H Perry; M Johnson; E K Perry
Neuroscience 1998;87(1):63-78.
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