Premium
P3‐372: Macrophage migration inhibitory factor in mild cognitive impairment and Alzheimer's disease
Author(s) -
Popp Julius
Publication year - 2008
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2008.05.1942
Subject(s) - macrophage migration inhibitory factor , pathogenesis , dementia , disease , neuroinflammation , medicine , cytokine , cerebrospinal fluid , immunology , cognitive decline , immune system , inflammation , alzheimer's disease , risk factor , psychology
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-a, IL-6 and IFN-c, 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-a, IL-6 and IFN-c, 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-a, IL-6 and IFN-c did not differ significantly between the groups. There was a correlation only between the concentrations of MIF and of TNF-a 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.