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Macrophage colony-stimulating factor (M-CSF) in plasma and CSF of patients with mild cognitive impairment and
C Laske1, E Stransky, N Hoffmann
1Department of Psychiatry and Psychotherapy, University of Tübingen, Osianderstr. 24, D-72076 Tübingen, Germany.
Abstract:
Macrophage colony-stimulating factor (M-CSF) is a hematopoietic growth factor that activates microglial cells, involved in phagocytosis of amyloid-beta (Abeta) in the brain. In the present study, we found in 50 patients with Alzheimer's disease (AD) significantly increased M-CSF plasma levels compared to 22 patients with mild cognitive impairment (MCI) and 35 age-matched healthy controls. In contrast, MCI patients showed significantly decreased M-CSF levels in cerebrospinal fluid (CSF) compared to AD patients and 20 patients with other non-inflammatory neurological disease (NIND). Analyzing the impact of Beta-amyloid 1-42 (Abeta 1-42), tau protein and M-CSF for differentiation between the groups we found that M-CSF, but not Abeta 1-42 and tau-protein is a significant parameter for distinction between MCI and NIND patients with 68.8% sensitivity and 75.0% specificity. M-CSF CSF levels < or = 357.8 pg/ml yielded 73.7% sensitivity and 75.0% specificity for diagnosing MCI patients in comparison with control subjects. In conclusion, our data indicate that M-CSF in CSF could be a putative biomarker for MCI.
Insights
Macrophage colony-stimulating factor (M-CSF) shows altered levels in Alzheimer's disease (AD) and mild cognitive impairment (MCI). Cerebrospinal fluid M-CSF may serve as a biomarker for distinguishing MCI from other neurological conditions.
Area of Science:
- Neuroscience
- Immunology
- Biochemistry
Background:
- Macrophage colony-stimulating factor (M-CSF) is a hematopoietic growth factor that activates microglial cells.
- Microglial activation and phagocytosis of amyloid-beta (Abeta) are implicated in Alzheimer's disease (AD) pathogenesis.
- M-CSF's role in neuroinflammation and its potential as a biomarker in cognitive decline warrant investigation.
Purpose of the Study:
- To investigate M-CSF levels in plasma and cerebrospinal fluid (CSF) across patient groups with AD, MCI, and healthy controls.
- To evaluate the diagnostic potential of M-CSF, Abeta 1-42, and tau protein in differentiating between MCI and other neurological diseases (NIND).
- To assess the utility of CSF M-CSF levels in diagnosing MCI compared to control subjects.
Main Methods:
- Plasma and CSF samples were collected from patients with AD, MCI, NIND, and age-matched healthy controls.
- M-CSF levels were measured in plasma and CSF using quantitative assays.
- Statistical analyses were performed to compare M-CSF levels between groups and to determine diagnostic accuracy (sensitivity and specificity) for M-CSF and other biomarkers.
Main Results:
- Significantly increased M-CSF plasma levels were observed in AD patients compared to MCI patients and healthy controls.
- MCI patients exhibited significantly decreased M-CSF levels in CSF compared to AD patients and NIND patients.
- M-CSF, but not Abeta 1-42 or tau protein, was a significant parameter for distinguishing MCI from NIND (68.8% sensitivity, 75.0% specificity).
- CSF M-CSF levels below or equal to 357.8 pg/ml showed 73.7% sensitivity and 75.0% specificity for diagnosing MCI versus controls.
Conclusions:
- M-CSF levels differ significantly in plasma and CSF across stages of cognitive decline and in comparison to neurological disease controls.
- CSF M-CSF demonstrates potential as a diagnostic biomarker for mild cognitive impairment (MCI).
- Further research is needed to validate M-CSF as a reliable biomarker for early detection and diagnosis of MCI.
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