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Abstract Details

Glial Fibrillary Acidic Protein in Multiple System Atrophy
Autonomic Disorders
P10 - Poster Session 10 (8:00 AM-9:00 AM)
7-003
To assess glial fibrillary acidic protein (GFAP) in cerebrospinal fluid (CSF) as diagnostic and/or progression marker for multiple system atrophy (MSA) among participants enrolled in a prospective, longitudinal study of early synucleinopathies.
Despite the recent discovery of novel biomarkers for MSA, the diagnosis remains challenging and there are no convincing markers of disease progression. GFAP has been proposed as a promising marker given the substantial glial pathology and evidence of its upregulation in MSA.

Well-characterized patients with early MSA (n=27; 15 MSA-C and 12 MSA-P), Parkinson’s disease (PD, n=16), and matched controls (CON, n=15) were included, and diagnoses confirmed using a CSF seed aggregation assay. GFAP and neurofilament light chain (NfL) were measured in CSF using a high sensitivity immunoassay at baseline, and in randomly selected MSA cases serially for 3 years. Subjects also underwent annual clinical and autonomic assessments, and structural and diffusion brain MRI with morphometric analysis.
GFAP was significantly higher in MSA compared to CON (1176±543 vs 869±421 pg/ml, p=0.02), but there was no statistical difference compared to PD (994±266 pg/ml), and there was considerable overlap between groups. Patients with MSA-C trended to have higher GFAP than MSA-P (p=0.07), and MSA-C - but not MSA-P - had significantly higher values than CON (p=0.01). In patients with serial measurements, there was no significant change over time. There was no significant association with clinical markers of disease severity or progression. However, structural MRI revealed a significant inverse correlation between cerebellar white matter volume and GFAP levels.

These findings demonstrate that GFAP is elevated in the CSF of patients with MSA but overlap with comparison groups limits its value as diagnostic marker. The elevation is driven by the MSA-C subtype which along with an association with the degree of cerebellar atrophy may suggest regional heterogeneity of the origin of GFAP in CSF.
Authors/Disclosures
Wolfgang Singer, MD, FAAN (Mayo Clinic)
PRESENTER 		Dr. Singer has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Biohaven. The institution of Dr. Singer has received personal compensation in the range of $10,000-$49,999 for serving as a Consultant for Lundbeck. Dr. Singer has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Ionis. Dr. Singer has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Yoda. Dr. Singer has received personal compensation in the range of $5,000-$9,999 for serving on a Scientific Advisory or Data Safety Monitoring board for Theravance. Dr. Singer has received personal compensation in the range of $5,000-$9,999 for serving on a Scientific Advisory or Data Safety Monitoring board for Ferrer. The institution of Dr. Singer has received research support from NIH. The institution of Dr. Singer has received research support from FDA. The institution of Dr. Singer has received research support from Michael J. Fox Foundation. Dr. Singer has received intellectual property interests from a discovery or technology relating to health care.
Ann M. Schmeichel Ann M. Schmeichel has nothing to disclose.
Pinaki P. Misra, PhD Dr. Misra has nothing to disclose.
Shannen Griffiths Miss Griffiths has received personal compensation for serving as an employee of Mayo Clinic.
Jennifer Anderson Jennifer Anderson has nothing to disclose.
David M. Sletten, MBA Mr. Sletten has nothing to disclose.
Tonette Gehrking Tonette Gehrking has nothing to disclose.
Jade Gehrking (Mayo Clinic, Neurology Dept) Jade Gehrking has nothing to disclose.
Prashanthi Vemuri, PhD (Mayo Clinic) The institution of Dr. Vemuri has received research support from NIH.
Phillip A. Low, MD, FAAN (Mayo Clinic) Dr. Low has nothing to disclose.