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Abstract Details

Cerebrospinal Fluid Inflammatory Markers Predict Subsequent Cognitive Decline in Alzheimer’s Disease
Aging, Dementia, and Behavioral Neurology
Aging and Dementia Posters (7:00 AM-5:00 PM)
053
There is evidence supporting that early neuroinflammatory markers including tumor necrosis factor (TNFalpha) and receptor (TNFR)-signaling, transforming growth factor beta (TGFbeta), interleukins (IL-21, IL-6, IL-7, IL-9, IL-10, IL-12p40), interferon gamma-induced protein-10 (IP-10), intercellular adhesion molecule (ICAM-1), and vascular cell adhesion molecule (VCAM-1) can promote brain aging and play role in early pathogenesis in Alzheimer’s Disease(AD). We hypothesized that inflammation induces the blood-brain barrier (BBB) impairment which is considered to be one of the core AD pathologies. However, it is still unclear whether neuroinflammatory markers can predict subsequent cognitive decline in the early stage of AD.
NA
We analyzed the baseline levels of TNFR(1-2), TGFbeta(1-2-3), IL-21, IL-6, IL-7, IL-9, IL-10, TNFalpha, IP-10, IL-12p40, ICAM-1, VCAM-1 in cerebrospinal fluid (CSF). The volume of white matter hyperintensity(WMH) was measured at baseline conventional MRI and added supplementarily to the inflammatory markers. The cognitively normal (CN) 40 patients were followed for 7-11 years from 2005 to 2016. They were divided into two groups based on subsequent clinical dementia rate (CDR): 1) Stable group who remained CN (n=25), and 2) Converters who were converted to mild cognitive impairment (MCI) (n=15). We compared the baseline neuroinflammatory levels between two groups.

In this retrospective longitudinal study, Converters had a higher CSF level of VCAM-1 among all the markers compared to the Stable group (p<0.001). Although the mean value of IL21 was higher in the Converters (15.1) compared to the Stable group (9.8), it did not reach statistical significance.



Our study demonstrated that VCAM-1 involved in the early pathogenesis of AD through BBB impairment, and which could be used as a marker of predicting cognitive decline, even a potential therapeutic target.
Authors/Disclosures
Zeynep Demir, MD (Neurocrine)
PRESENTER
Dr. Demir has nothing to disclose.
No disclosure on file
Min Jiangyong, MD (Michigan State Universtiy) No disclosure on file