Prognostic Role of CSF β-amyloid 1–42/1–40 Ratio in Patients Affected by Amyotrophic Lateral Sclerosis
Authors:
- Tiziana CollettiTiziana Colletti
- Luisa AgnelloLuisa Agnello
- Rossella SpataroRSRossella Spataro
- Lavinia GuccioneLGLavinia Guccione
- Antonietta NotaroANAntonietta Notaro
- Bruna Lo SassoBSBruna Lo Sasso
- Valeria BlandinoVBValeria Blandino
- Fabiola GrazianoFGFabiola Graziano
- Caterina Maria GambinoCGCaterina Maria Gambino
- Rosaria Vincenza GiglioRGRosaria Vincenza Giglio
- Giulia BivonaGiulia Bivona
- Vincenzo La BellaVincenzo La Bella
Open Access
- 27 February 2021
- journal article
- research article
- Published by MDPI AG in Brain Sciences
- Vol. 11 (3) , 302
Abstract
The involvement of β-amyloid (Aβ) in the pathogenesis of amyotrophic lateral sclerosis (ALS) has been widely discussed and its role in the disease is still a matter of debate. Aβ accumulates in the cortex and the anterior horn neurons of ALS patients and seems to affect their survival. To clarify the role of cerebrospinal fluid (CSF) Aβ 1–42 and Aβ 42/40 ratios as a potential prognostic biomarker for ALS, we performed a retrospective observational study on a cohort of ALS patients who underwent a lumbar puncture at the time of the diagnosis. CSF Aβ 1–40 and Aβ 1–42 ratios were detected by chemiluminescence immunoassay and their values were correlated with clinical features. We found a significant correlation of the Aβ 42/40 ratio with age at onset and Mini Mental State Examination (MMSE) scores. No significant correlation of Aβ 1–42 or Aβ 42/40 ratios to the rate of progression of the disease were found. Furthermore, when we stratified patients according to Aβ 1–42 concentration and the Aβ 42/40 ratio, we found that patients with a lower Aβ 42/40 ratio showed a shorter survival. Our results support the hypothesis that Aβ 1–42 could be involved in some pathogenic mechanism of ALS and we suggest the Aβ 42/40 ratio as a potential prognostic biomarker.Keywords
This publication has 35 references indexed in Scilit:
- Expanded GGGGCC Hexanucleotide Repeat in Noncoding Region of C9ORF72 Causes Chromosome 9p-Linked FTD and ALSNeuron, 2011
- A Hexanucleotide Repeat Expansion in C9ORF72 Is the Cause of Chromosome 9p21-Linked ALS-FTDNeuron, 2011
- Relationship between ALS and the degree of cognitive impairment, markers of neurodegeneration and predictors for poor outcome. A prospective studyEuropean Journal of Neurology, 2009
- Beta-Amyloid Deposition and the Aging BrainNeuropsychology Review, 2009
- Cerebrospinal fluid tau protein is not a biological marker in amyotrophic lateral sclerosisEuropean Journal of Neurology, 2009
- Prognostic factors in ALS: A critical reviewAmyotrophic Lateral Sclerosis, 2009
- Intracellular amyloid beta interacts with SOD1 and impairs the enzymatic activity of SOD1: implications for the pathogenesis of amyotrophic lateral sclerosisExperimental & Molecular Medicine, 2009
- Overexpression of Aβ is associated with acceleration of onset of motor impairment and superoxide dismutase 1 aggregation in an amyotrophic lateral sclerosis mouse modelAging Cell, 2006
- β-amyloid 42 accumulation in the lumbar spinal cord motor neurons of amyotrophic lateral sclerosis patientsNeurobiology of Disease, 2005
- A role for neurofilaments in the pathogenesis of amyotrophic lateral sclerosisBiochemistry and Cell Biology, 1995