No changes in central quinolinic acid levels in Alzheimer's disease

1989 ◽  
Vol 105 (1-2) ◽  
pp. 233-238 ◽  
Author(s):  
M.M. Mourdian ◽  
M.P. Heyes ◽  
J.-B. Pan ◽  
I.J.E. Heuser ◽  
S.P. Markey ◽  
...  
Author(s):  
Gilles J. Guillemin ◽  
Kieran R. Williams ◽  
Danielle G. Smith ◽  
George A. Smythe ◽  
Juliana Croitoru-Lamoury ◽  
...  

2007 ◽  
Vol 1304 ◽  
pp. 404-408 ◽  
Author(s):  
Gilles J. Guillemin ◽  
Bruce J. Brew ◽  
Claire E. Noonan ◽  
Toby G. Knight ◽  
George A. Smythe ◽  
...  

2017 ◽  
Vol 34 (1) ◽  
pp. 147-163 ◽  
Author(s):  
Paula Pierozan ◽  
Helena Biasibetti-Brendler ◽  
Felipe Schmitz ◽  
Fernanda Ferreira ◽  
Carlos Alexandre Netto ◽  
...  

2010 ◽  
Vol 2010 ◽  
pp. 1-6 ◽  
Author(s):  
S. Duleu ◽  
A. Mangas ◽  
F. Sevin ◽  
B. Veyret ◽  
A. Bessede ◽  
...  

In Alzheimer's disease, indoleamine 2,3-dioxygenase and tryptophan hydroxylase are known to induce an overproduction of neurotoxic compounds, such as quinolinic acid and 3-hydroxykynurenine from the former, and 5-hydroxytryptophol and 5-methoxytryptophol from the latter. Other compounds, such as kynurenic acid, serotonin, and melatonin are produced via the same pathways. An improved ELISA method identified circulating antibodies directed against these compounds, linked to proteins, as previously described for other chronic diseases. This describes how only the A isotype of circulating immunoglobulins recognized a pattern of conjugated tryptophan metabolites in the sera of Alzheimer patients. These data indirectly confirmed the involvement of tryptophan derivatives in the pathogenic processes of Alzheimer's disease. Further studies are required to evaluate the relevance of these antibody patterns in monitoring this disease.


2012 ◽  
Vol 8 (4S_Part_18) ◽  
pp. P656-P656
Author(s):  
Alato Okuno ◽  
Tatsuya Yoshimi ◽  
Kayo Adachi ◽  
Ryuta Mikawa ◽  
Akiko Takayanagi ◽  
...  

2005 ◽  
Vol 31 (4) ◽  
pp. 395-404 ◽  
Author(s):  
G. J. Guillemin ◽  
B. J. Brew ◽  
C. E. Noonan ◽  
O. Takikawa ◽  
K. M. Cullen

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