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Decreased levels of intrathecal interleukin 1 receptor antagonist in Alzheimer's disease

Tarkowski, E; Liljeroth, A M; Minthon, Lennart LU and Blennow, K (2001) In Dementia and Geriatric Cognitive Disorders 12(5). p.314-317
Abstract
A growing body of evidence points out the potential role of inflammatory mechanisms in the pathophysiology of brain damage in dementia. In previous studies, we have demonstrated intrathecal production of the proinflammatory cytokine tumor necrosis factor (TNF)alpha in patients with Alzheimer's disease (AD). The aim of the present study was to investigate the downstream products of TNF-alpha expression including interleukin (IL)1beta and its naturally occurring antagonist IL-1 receptor agonist (ra) in patients with AD. The cytokine levels were related to neuronal damage, as measured by intrathecal tau and beta-amyloid concentration and certain clinical features of the disease. Fifty-two patients with AD and 25 healthy controls were analyzed... (More)
A growing body of evidence points out the potential role of inflammatory mechanisms in the pathophysiology of brain damage in dementia. In previous studies, we have demonstrated intrathecal production of the proinflammatory cytokine tumor necrosis factor (TNF)alpha in patients with Alzheimer's disease (AD). The aim of the present study was to investigate the downstream products of TNF-alpha expression including interleukin (IL)1beta and its naturally occurring antagonist IL-1 receptor agonist (ra) in patients with AD. The cytokine levels were related to neuronal damage, as measured by intrathecal tau and beta-amyloid concentration and certain clinical features of the disease. Fifty-two patients with AD and 25 healthy controls were analyzed with respect to cerebrospinal fluid (CSF) levels of IL-1beta and IL-1ra. CSF IL-1beta was neither detectable in CSF of AD nor in control CSF. In contrast, a significantly lower (p < 0.01) number of patients (24 of 49) than of controls (20 of 24) showed detectable levels of IL-1ra in the CSF. The intrathecal levels of IL-1ra were significantly lower in patients with AD than in the controls. Our study demonstrates a decreased production of the anti-inflammatory compound IL-1ra, suggesting a propensity towards inflammation in patients with AD. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Dementia and Geriatric Cognitive Disorders
volume
12
issue
5
pages
314 - 317
publisher
Karger
external identifiers
  • wos:000170289000004
  • scopus:0034959833
ISSN
1420-8008
DOI
10.1159/000051276
language
English
LU publication?
yes
id
e5431010-de3c-47b8-803b-f6e00f3e7feb (old id 1297285)
date added to LUP
2009-07-15 10:09:41
date last changed
2018-01-07 05:39:24
@article{e5431010-de3c-47b8-803b-f6e00f3e7feb,
  abstract     = {A growing body of evidence points out the potential role of inflammatory mechanisms in the pathophysiology of brain damage in dementia. In previous studies, we have demonstrated intrathecal production of the proinflammatory cytokine tumor necrosis factor (TNF)alpha in patients with Alzheimer's disease (AD). The aim of the present study was to investigate the downstream products of TNF-alpha expression including interleukin (IL)1beta and its naturally occurring antagonist IL-1 receptor agonist (ra) in patients with AD. The cytokine levels were related to neuronal damage, as measured by intrathecal tau and beta-amyloid concentration and certain clinical features of the disease. Fifty-two patients with AD and 25 healthy controls were analyzed with respect to cerebrospinal fluid (CSF) levels of IL-1beta and IL-1ra. CSF IL-1beta was neither detectable in CSF of AD nor in control CSF. In contrast, a significantly lower (p &lt; 0.01) number of patients (24 of 49) than of controls (20 of 24) showed detectable levels of IL-1ra in the CSF. The intrathecal levels of IL-1ra were significantly lower in patients with AD than in the controls. Our study demonstrates a decreased production of the anti-inflammatory compound IL-1ra, suggesting a propensity towards inflammation in patients with AD.},
  author       = {Tarkowski, E and Liljeroth, A M and Minthon, Lennart and Blennow, K},
  issn         = {1420-8008},
  language     = {eng},
  number       = {5},
  pages        = {314--317},
  publisher    = {Karger},
  series       = {Dementia and Geriatric Cognitive Disorders},
  title        = {Decreased levels of intrathecal interleukin 1 receptor antagonist in Alzheimer's disease},
  url          = {http://dx.doi.org/10.1159/000051276},
  volume       = {12},
  year         = {2001},
}