Macrophage migration inhibitory factor in mild cognitive impairment and Alzheimer’s disease
Inflammatory processes may substantially contribute to the cerebral pathology in Alzheimer’s disease (AD) and accelerate the disease progression. The macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine which promotes the production of several inflammatory mediators such as TN...
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| Published in | Journal of psychiatric research Vol. 43; no. 8; pp. 749 - 753 |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Kidlington
Elsevier Ltd
01.05.2009
Elsevier |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0022-3956 1879-1379 1879-1379 |
| DOI | 10.1016/j.jpsychires.2008.10.006 |
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| Abstract | Inflammatory processes may substantially contribute to the cerebral pathology in Alzheimer’s disease (AD) and accelerate the disease progression. The macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine which promotes the production of several inflammatory mediators such as TNF-α, IL-6 and IFN-γ, and plays a central regulatory role in the pathogenesis of several inflammatory and autoimmune diseases. There is now first evidence that MIF may be involved in the neuroinflammation in AD. To determine whether MIF production is up-regulated early in the course of AD, we compared the levels of MIF assessed by ELISA in the cerebrospinal fluid (CSF) of 31 patients with AD, 28 patients with amnestic mild cognitive impairment (MCI), and 19 subjects without cognitive deficits. Additionally, we measured the CSF concentrations of the inflammatory mediators TNF-α, IL-6 and IFN-γ, which are thought to be both up-regulated by MIF and involved in the pathophysiology of AD. CSF MIF concentrations were significantly increased in AD (
p
=
0.003) and MCI patients (
p
<
0.001) compared to controls. The levels of TNF-α, IL-6 and IFN-γ did not differ significantly between the groups. There was a correlation only between the concentrations of MIF and of TNF-α in the AD group (
r
=
0.407;
p
=
0.023). These results demonstrate increased MIF production in AD and MCI suggesting that MIF may be involved in the occurring neuroinflammatory process at a clinical pre-dementia disease stage. |
|---|---|
| AbstractList | Inflammatory processes may substantially contribute to the cerebral pathology in Alzheimer's disease (AD) and accelerate the disease progression. The macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine which promotes the production of several inflammatory mediators such as TNF-[alpha], IL-6 and IFN-[gamma], and plays a central regulatory role in the pathogenesis of several inflammatory and autoimmune diseases. There is now first evidence that MIF may be involved in the neuroinflammation in AD. To determine whether MIF production is up-regulated early in the course of AD, we compared the levels of MIF assessed by ELISA in the cerebrospinal fluid (CSF) of 31 patients with AD, 28 patients with amnestic mild cognitive impairment (MCI), and 19 subjects without cognitive deficits. Additionally, we measured the CSF concentrations of the inflammatory mediators TNF-[alpha], IL-6 and IFN-[gamma], which are thought to be both up-regulated by MIF and involved in the pathophysiology of AD. CSF MIF concentrations were significantly increased in AD (p = 0.003) and MCI patients (p < 0.001) compared to controls. The levels of TNF-[alpha], IL-6 and IFN-[gamma] did not differ significantly between the groups. There was a correlation only between the concentrations of MIF and of TNF-[alpha] in the AD group (r = 0.407; p = 0.023). These results demonstrate increased MIF production in AD and MCI suggesting that MIF may be involved in the occurring neuroinflammatory process at a clinical pre-dementia disease stage. [Copyright Elsevier Ltd.] Inflammatory processes may substantially contribute to the cerebral pathology in Alzheimer’s disease (AD) and accelerate the disease progression. The macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine which promotes the production of several inflammatory mediators such as TNF-α, IL-6 and IFN-γ, and plays a central regulatory role in the pathogenesis of several inflammatory and autoimmune diseases. There is now first evidence that MIF may be involved in the neuroinflammation in AD. To determine whether MIF production is up-regulated early in the course of AD, we compared the levels of MIF assessed by ELISA in the cerebrospinal fluid (CSF) of 31 patients with AD, 28 patients with amnestic mild cognitive impairment (MCI), and 19 subjects without cognitive deficits. Additionally, we measured the CSF concentrations of the inflammatory mediators TNF-α, IL-6 and IFN-γ, which are thought to be both up-regulated by MIF and involved in the pathophysiology of AD. CSF MIF concentrations were significantly increased in AD ( p = 0.003) and MCI patients ( p < 0.001) compared to controls. The levels of TNF-α, IL-6 and IFN-γ did not differ significantly between the groups. There was a correlation only between the concentrations of MIF and of TNF-α in the AD group ( r = 0.407; p = 0.023). These results demonstrate increased MIF production in AD and MCI suggesting that MIF may be involved in the occurring neuroinflammatory process at a clinical pre-dementia disease stage. Inflammatory processes may substantially contribute to the cerebral pathology in Alzheimer's disease (AD) and accelerate the disease progression. The macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine which promotes the production of several inflammatory mediators such as TNF-alpha, IL-6 and IFN-gamma, and plays a central regulatory role in the pathogenesis of several inflammatory and autoimmune diseases. There is now first evidence that MIF may be involved in the neuroinflammation in AD. To determine whether MIF production is up-regulated early in the course of AD, we compared the levels of MIF assessed by ELISA in the cerebrospinal fluid (CSF) of 31 patients with AD, 28 patients with amnestic mild cognitive impairment (MCI), and 19 subjects without cognitive deficits. Additionally, we measured the CSF concentrations of the inflammatory mediators TNF-alpha, IL-6 and IFN-gamma, which are thought to be both up-regulated by MIF and involved in the pathophysiology of AD. CSF MIF concentrations were significantly increased in AD (p=0.003) and MCI patients (p<0.001) compared to controls. The levels of TNF-alpha, IL-6 and IFN-gamma did not differ significantly between the groups. There was a correlation only between the concentrations of MIF and of TNF-alpha in the AD group (r=0.407; p=0.023). These results demonstrate increased MIF production in AD and MCI suggesting that MIF may be involved in the occurring neuroinflammatory process at a clinical pre-dementia disease stage. Abstract Inflammatory processes may substantially contribute to the cerebral pathology in Alzheimer’s disease (AD) and accelerate the disease progression. The macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine which promotes the production of several inflammatory mediators such as TNF-α, IL-6 and IFN-γ, and plays a central regulatory role in the pathogenesis of several inflammatory and autoimmune diseases. There is now first evidence that MIF may be involved in the neuroinflammation in AD. To determine whether MIF production is up-regulated early in the course of AD, we compared the levels of MIF assessed by ELISA in the cerebrospinal fluid (CSF) of 31 patients with AD, 28 patients with amnestic mild cognitive impairment (MCI), and 19 subjects without cognitive deficits. Additionally, we measured the CSF concentrations of the inflammatory mediators TNF-α, IL-6 and IFN-γ, which are thought to be both up-regulated by MIF and involved in the pathophysiology of AD. CSF MIF concentrations were significantly increased in AD ( p = 0.003) and MCI patients ( p < 0.001) compared to controls. The levels of TNF-α, IL-6 and IFN-γ did not differ significantly between the groups. There was a correlation only between the concentrations of MIF and of TNF-α in the AD group ( r = 0.407; p = 0.023). These results demonstrate increased MIF production in AD and MCI suggesting that MIF may be involved in the occurring neuroinflammatory process at a clinical pre-dementia disease stage. Inflammatory processes may substantially contribute to the cerebral pathology in Alzheimer's disease (AD) and accelerate the disease progression. The macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine which promotes the production of several inflammatory mediators such as TNF-alpha, IL-6 and IFN-gamma, and plays a central regulatory role in the pathogenesis of several inflammatory and autoimmune diseases. There is now first evidence that MIF may be involved in the neuroinflammation in AD. To determine whether MIF production is up-regulated early in the course of AD, we compared the levels of MIF assessed by ELISA in the cerebrospinal fluid (CSF) of 31 patients with AD, 28 patients with amnestic mild cognitive impairment (MCI), and 19 subjects without cognitive deficits. Additionally, we measured the CSF concentrations of the inflammatory mediators TNF-alpha, IL-6 and IFN-gamma, which are thought to be both up-regulated by MIF and involved in the pathophysiology of AD. CSF MIF concentrations were significantly increased in AD (p=0.003) and MCI patients (p<0.001) compared to controls. The levels of TNF-alpha, IL-6 and IFN-gamma did not differ significantly between the groups. There was a correlation only between the concentrations of MIF and of TNF-alpha in the AD group (r=0.407; p=0.023). These results demonstrate increased MIF production in AD and MCI suggesting that MIF may be involved in the occurring neuroinflammatory process at a clinical pre-dementia disease stage.Inflammatory processes may substantially contribute to the cerebral pathology in Alzheimer's disease (AD) and accelerate the disease progression. The macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine which promotes the production of several inflammatory mediators such as TNF-alpha, IL-6 and IFN-gamma, and plays a central regulatory role in the pathogenesis of several inflammatory and autoimmune diseases. There is now first evidence that MIF may be involved in the neuroinflammation in AD. To determine whether MIF production is up-regulated early in the course of AD, we compared the levels of MIF assessed by ELISA in the cerebrospinal fluid (CSF) of 31 patients with AD, 28 patients with amnestic mild cognitive impairment (MCI), and 19 subjects without cognitive deficits. Additionally, we measured the CSF concentrations of the inflammatory mediators TNF-alpha, IL-6 and IFN-gamma, which are thought to be both up-regulated by MIF and involved in the pathophysiology of AD. CSF MIF concentrations were significantly increased in AD (p=0.003) and MCI patients (p<0.001) compared to controls. The levels of TNF-alpha, IL-6 and IFN-gamma did not differ significantly between the groups. There was a correlation only between the concentrations of MIF and of TNF-alpha in the AD group (r=0.407; p=0.023). These results demonstrate increased MIF production in AD and MCI suggesting that MIF may be involved in the occurring neuroinflammatory process at a clinical pre-dementia disease stage. |
| Author | Deuster, Oliver Jessen, Frank Noelker, Carmen Bacher, Michael Popp, Julius Kölsch, Heike Dodel, Richard |
| Author_xml | – sequence: 1 givenname: Julius surname: Popp fullname: Popp, Julius email: Julius.Popp@ukb.uni-bonn.de organization: University of Bonn, Department of Psychiatry, Sigmund-Freud-Strasse 25, 53105 Bonn, Germany – sequence: 2 givenname: Michael surname: Bacher fullname: Bacher, Michael organization: University of Marburg, Department of Neurology, Rudolf-Bultmannstr. 8, 35039 Marburg, Germany – sequence: 3 givenname: Heike surname: Kölsch fullname: Kölsch, Heike organization: University of Bonn, Department of Psychiatry, Sigmund-Freud-Strasse 25, 53105 Bonn, Germany – sequence: 4 givenname: Carmen surname: Noelker fullname: Noelker, Carmen organization: University of Marburg, Department of Neurology, Rudolf-Bultmannstr. 8, 35039 Marburg, Germany – sequence: 5 givenname: Oliver surname: Deuster fullname: Deuster, Oliver organization: University of Marburg, Department of Neurology, Rudolf-Bultmannstr. 8, 35039 Marburg, Germany – sequence: 6 givenname: Richard surname: Dodel fullname: Dodel, Richard organization: University of Marburg, Department of Neurology, Rudolf-Bultmannstr. 8, 35039 Marburg, Germany – sequence: 7 givenname: Frank surname: Jessen fullname: Jessen, Frank organization: University of Bonn, Department of Psychiatry, Sigmund-Freud-Strasse 25, 53105 Bonn, Germany |
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| Keywords | Macrophage migration inhibitory factor Neuroinflammation Cerebrospinal fluid Amnestic mild cognitive impairment Alzheimer’s disease Memory disorder Nervous system diseases Cognitive disorder Alzheimer disease Cerebral disorder Central nervous system disease Degenerative disease mild cognitive impairment Amnesia Inhibition Neurological disorder Alzheimer's disease Macrophage |
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| Snippet | Inflammatory processes may substantially contribute to the cerebral pathology in Alzheimer’s disease (AD) and accelerate the disease progression. The... Abstract Inflammatory processes may substantially contribute to the cerebral pathology in Alzheimer’s disease (AD) and accelerate the disease progression. The... Inflammatory processes may substantially contribute to the cerebral pathology in Alzheimer's disease (AD) and accelerate the disease progression. The... |
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| SubjectTerms | Adult and adolescent clinical studies Aged Aged, 80 and over Alzheimer Disease - cerebrospinal fluid Alzheimer Disease - immunology Alzheimer's disease Amnestic mild cognitive impairment Autoimmune disorders Biological and medical sciences Cerebrospinal fluid Cognition Disorders - cerebrospinal fluid Cognition Disorders - immunology Cognitive impairment Control Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Disorders of higher nervous function. Focal brain diseases. Central vestibular syndrome and deafness. Brain stem syndromes Enzyme-Linked Immunosorbent Assay Female Geriatrics Humans Interferon-gamma - cerebrospinal fluid Interleukin-6 - cerebrospinal fluid Macrophage migration inhibitory factor Macrophage Migration-Inhibitory Factors - cerebrospinal fluid Macrophage Migration-Inhibitory Factors - immunology Male Medical sciences Middle Aged Migration Nervous system (semeiology, syndromes) Neuroinflammation Neurology Organic mental disorders. Neuropsychology Pathology Psychiatry Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Severity of Illness Index Tumor Necrosis Factor-alpha - cerebrospinal fluid Up-Regulation |
| Title | Macrophage migration inhibitory factor in mild cognitive impairment and Alzheimer’s disease |
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