CCL11 is increased in the CNS in chronic traumatic encephalopathy but not in Alzheimer’s disease
Year: 2017
Type: article
Study design: Observational Study
Abstract: CCL11, a protein previously associated with age-associated cognitive decline, is observed to be increased in the brain and cerebrospinal fluid (CSF) in chronic traumatic encephalopathy (CTE) compared to Alzheimer's disease (AD). Using a cohort of 23 deceased American football players with neuropathologically verified CTE, 50 subjects with neuropathologically diagnosed AD, and 18 non-athlete controls, CCL11 was measured with ELISA in the dorsolateral frontal cortex (DLFC) and CSF. CCL11 levels were significantly increased in the DLFC in subjects with CTE (fold change = 1.234, p < 0.050) compared to non-athlete controls and AD subjects with out a history of head trauma. This increase was also seen to correlate with years of exposure to American football (β = 0.426, p = 0.048) independent of age (β = -0.046, p = 0.824). Preliminary analyses of a subset of subjects with available post-mortem CSF showed a trend for increased CCL11 among individuals with CTE (p = 0.069) mirroring the increase in the DLFC. Furthermore, an association between CSF CCL11 levels and the number of years exposed to football (β = 0.685, p = 0.040) was observed independent of age (β = -0.103, p = 0.716). Finally, a receiver operating characteristic (ROC) curve analysis demonstrated CSF CCL11 accurately distinguished CTE subjects from non-athlete controls and AD subjects (AUC = 0.839, 95% CI 0.62-1.058, p = 0.028). Overall, the current findings provide preliminary evidence that CCL11 may be a novel target for future CTE biomarker studies.
Source: PLoS ONE
Language: English
Subfield: Epidemiology
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $2,382
Funders: U.S. Department of Defense, U.S. Department of Veterans Affairs, Alzheimer's Association, Andlinger Family Foundation, Concussion Legacy Foundation, National Institutes of Health, National Institute on Aging, National Heart, Lung, and Blood Institute, National Institute of Neurological Disorders and Stroke
Awards: G1156429883, G1490530680, G1949952796, G250621538, G3082176553, G3667269547, G4300776172, Magnetic Resonance Spectroscopy as a Biomarker for Chronic Traumatic Encephalopathy, Genetic and Neuropsychological Heterogeneity in Alzheimer's Disease, G5164707915, G5281659474, G633564771, The Framingham Heart Study, CTE and Posttraumatic Neurodegeneration: Neuropathology and Ex Vivo Imaging, Boston University Alzheimer's Disease Center, Epigenetic changes in synaptic and inflammatory genes involved in the age-dependent development of Alzheimer's disease pathologies andcognitive decline, Epidemiology of Dementia in the Framingham Study, G9000124674, Tau Pathology in CTE vs. Alzheimer's Disease: Microvasculopathy and Neuroinflammation
OpenAlex ID: W2758061377
