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Muscle and not neuronal biomarkers correlate with severity in spinal and bulbar muscular atrophy

Artikel i vetenskaplig tidskrift
Författare V. Lombardi
G. Querin
O. J. Ziff
L. Zampedri
I. Martinelli
C. Heller
M. Foiani
C. Bertolin
C. H. Lu
B. Malik
K. Allen
C. Rinaldi
Henrik Zetterberg
A. Heslegrave
L. Greensmith
M. Hanna
G. Soraru
A. Malaspina
P. Fratta
Publicerad i Neurology
Volym 92
Nummer/häfte 11
Sidor E1205-E1211
ISSN 0028-3878
Publiceringsår 2019
Publicerad vid Institutionen för neurovetenskap och fysiologi
Sidor E1205-E1211
Språk en
Länkar dx.doi.org/10.1212/wnl.000000000000...
Ämnesord neurofilament light-chain, androgen receptor, skeletal-muscle, neuronopathy, expression, pathology, creatine, features, scale, Neurosciences & Neurology, ates of america, v104, p18259
Ämneskategorier Neurovetenskap

Sammanfattning

Objective To determine whether blood biomarkers of neuronal damage (neurofilament light chain [NfL]), muscle damage (creatine kinase [CK]), and muscle mass (creatinine) are altered in spinal and bulbar muscular atrophy (SBMA) and can be used as biomarkers for disease severity. In this multicenter longitudinal prospective study, plasma and serum were collected from 2 cohorts of patients with SBMA in London, United Kingdom (n = 50), and Padova, Italy (n = 43), along with disease (amyotrophic lateral sclerosis [ALS]) and healthy controls, and levels of plasma and serum NfL, CK, and creatinine were measured. Disease severity was assessed by the SBMA Functional Rating Scale and the Adult Myopathy Assessment Tool at baseline and 12 and 24 months. Blood NfL concentrations were increased in ALS samples, but were unchanged in both SBMA cohorts, were stable after 12 and 24 months, and were not correlated with clinical severity. Normal NfL levels were also found in a well-established mouse model of SBMA. Conversely, CK concentrations were significantly raised in SBMA compared with ALS samples, and were not correlated to the clinical measures. Creatinine concentrations were significantly reduced in SBMA, and strongly and significantly correlated with disease severity. While muscle damage and muscle mass biomarkers are abnormal in SBMA, axonal damage markers are unchanged, highlighting the relevant primary role of skeletal muscle in disease pathogenesis. Creatinine, but not CK, correlated with disease severity, confirming its role as a valuable biomarker in SBMA.

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