Premium
P4‐282: DEMOGRAPHIC FACTORS INFLUENCE PARTICIPATION IN LUMBAR PUNCTURES
Author(s) -
Blazel Madeleine,
Lazar Karen K.,
Van Hulle Carol A.,
Cole Aleshia,
Spalitta Alice,
Davenport Nancy J.,
Wahoske Michelle L.,
Illingworth Chuck,
Blazel Hanna,
Asthana Sanjay,
Johnson Sterling C.,
Carlsson Cynthia M.
Publication year - 2018
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.2018.07.104
Subject(s) - medicine , body mass index , logistic regression , family history , demography , ethnic group , waist , disease , gerontology , sociology , anthropology
Calgary (Canada); or Charit e Hospital and University Hospital Magdeburg (Germany). Biomarkers of neuronal injury (total tau, VILIP-1), inflammation (YKL-40), and neurotransmission (neurogranin, SNAP-25) were compared between patients and controls (univariate ANCOVA), controlling for age. Results: Median ageat-symptomatic onset of AME was 30.5 years (range, 11-85); 34/ 46 (74%) patients were female. Patients with NMDAR encephalitis were younger (27 years, 4.0-41.8) than patients with LGI1/ CASPR2 AME (70.4 years, 60.6-83.2; p<0.001). Markers of neuronal injury were similar (mean total tau [95%CI]: 22.6 pg/ml [16.8-28.5]; vs. 18.2 pg/ml [12.9-23.4]; p1⁄40.27) or decreased (VILIP-1: 47.2 pg/ml [34.5-59.8]; vs. 124.3 pg/ml [113.0-135.6]; p<0.001) in the CSF of AME patients versus controls. The neuroinflammatory biomarker YKL-40 was elevated in AME patient CSF (YKL-40: 315.0 pg/ml [272.0-358.1] vs. 177.7 pg/ml [139.6-215.9]; p<0.001), while markers of neurotransmission were decreased (SNAP-25: 1.63 pg/ml [1.29-1.97] vs. 3.22 pg/ml [2.92-3.53], p<0.001; neurogranin: 615.3 pg/ml [375-854.7] vs. pg/ml 1504.8 [1290.2-1719.3], p<0.001). VILIP-1 levels differentiated patients with AME associated with NMDAR (27.0 pg/ml [12.9-41.1]) from LGI1/CASPR2 autoantibodies (84.5 pg/ml [47.1-121.8]; p1⁄40.02). No other biomarker differences were observed between AME patients. Conclusions:Biofluid biomarkers validated in patients with neurodegenerative dementing illnesses may be applied to improve diagnosis and predict outcomes in patients with other causes of cognitive impairment. Specifically, these biomarkers suggest that neuronal integrity is acutely maintained in AME patients. Low-levels of biomarkers of neurotransmission may reflect antibody-mediated internalization of cell-surface receptors, and may represent an acute correlate of autoimmune-mediated synaptic dysfunction underlying cognitive sequelae in recovering patients.