Aβ1-42 induces production of quinolinic acid by human macrophages and microglia

Gilles J. Guillemin; George A. Smythe; Laura A. Veas; Osamu Takikawa; Bruce J. Brew

Aβ1-42 induces production of quinolinic acid by human macrophages and microglia

Gilles J. Guillemin^*, George A. Smythe, Laura A. Veas, Osamu Takikawa, Bruce J. Brew

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

5 Citations (Scopus)

Abstract

We hypothesized that the tryptophan catabolites produced through the kynurenine pathway (KP), and more particularly the excitotoxin quinolinic acid (QUIN), may play an important role in the pathogenesis of Alzheimer's disease (AD). In this study, we demonstrated that aggregated amyloid peptide Aβ1-42 induced indoleamine 2,3-dioxygenase (IDO) expression and resulted in a significant increase in production of QUIN by human primary macrophages and microglia. In contrast, Aβ1-40 and prion peptide (PrP) 106-126 did not induce any significant increase in QUIN production. These data imply that local QUIN production may be one of the factors involved in the pathogenesis of neuronal damage in AD.

Original language	English
Pages (from-to)	2311-2315
Number of pages	5
Journal	NeuroReport
Volume	14
Issue number	18
Publication status	Published - 2003
Externally published	Yes

Keywords

3-dioxygenase
Aβ1-42
Alzheimer's disease
human
indoleamine 2
macrophages
microglia
quinolinic acid

Cite this

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title = "Aβ1-42 induces production of quinolinic acid by human macrophages and microglia",

abstract = "We hypothesized that the tryptophan catabolites produced through the kynurenine pathway (KP), and more particularly the excitotoxin quinolinic acid (QUIN), may play an important role in the pathogenesis of Alzheimer's disease (AD). In this study, we demonstrated that aggregated amyloid peptide Aβ1-42 induced indoleamine 2,3-dioxygenase (IDO) expression and resulted in a significant increase in production of QUIN by human primary macrophages and microglia. In contrast, Aβ1-40 and prion peptide (PrP) 106-126 did not induce any significant increase in QUIN production. These data imply that local QUIN production may be one of the factors involved in the pathogenesis of neuronal damage in AD.",

keywords = "3-dioxygenase, Aβ1-42, Alzheimer's disease, human, indoleamine 2, macrophages, microglia, quinolinic acid",

author = "Guillemin, {Gilles J.} and Smythe, {George A.} and Veas, {Laura A.} and Osamu Takikawa and Brew, {Bruce J.}",

year = "2003",

language = "English",

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TY - JOUR

T1 - Aβ1-42 induces production of quinolinic acid by human macrophages and microglia

AU - Guillemin, Gilles J.

AU - Smythe, George A.

AU - Veas, Laura A.

AU - Takikawa, Osamu

AU - Brew, Bruce J.

PY - 2003

Y1 - 2003

N2 - We hypothesized that the tryptophan catabolites produced through the kynurenine pathway (KP), and more particularly the excitotoxin quinolinic acid (QUIN), may play an important role in the pathogenesis of Alzheimer's disease (AD). In this study, we demonstrated that aggregated amyloid peptide Aβ1-42 induced indoleamine 2,3-dioxygenase (IDO) expression and resulted in a significant increase in production of QUIN by human primary macrophages and microglia. In contrast, Aβ1-40 and prion peptide (PrP) 106-126 did not induce any significant increase in QUIN production. These data imply that local QUIN production may be one of the factors involved in the pathogenesis of neuronal damage in AD.

AB - We hypothesized that the tryptophan catabolites produced through the kynurenine pathway (KP), and more particularly the excitotoxin quinolinic acid (QUIN), may play an important role in the pathogenesis of Alzheimer's disease (AD). In this study, we demonstrated that aggregated amyloid peptide Aβ1-42 induced indoleamine 2,3-dioxygenase (IDO) expression and resulted in a significant increase in production of QUIN by human primary macrophages and microglia. In contrast, Aβ1-40 and prion peptide (PrP) 106-126 did not induce any significant increase in QUIN production. These data imply that local QUIN production may be one of the factors involved in the pathogenesis of neuronal damage in AD.

KW - 3-dioxygenase

KW - Aβ1-42

KW - Alzheimer's disease

KW - human

KW - indoleamine 2

KW - macrophages

KW - microglia

KW - quinolinic acid

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M3 - Article

AN - SCOPUS:85026152315

SN - 0959-4965

VL - 14

SP - 2311

EP - 2315

JO - NeuroReport

JF - NeuroReport

IS - 18

ER -

Aβ1-42 induces production of quinolinic acid by human macrophages and microglia

Abstract

Keywords

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