Anti-neural antibodies in serum and cerebrospinal fluid of amyotrophic lateral sclerosis (ALS) patients

Citation
I. Niebroj-dobosz et al., Anti-neural antibodies in serum and cerebrospinal fluid of amyotrophic lateral sclerosis (ALS) patients, ACT NEUR SC, 100(4), 1999, pp. 238-243
Citations number
42
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
ACTA NEUROLOGICA SCANDINAVICA
ISSN journal
00016314 → ACNP
Volume
100
Issue
4
Year of publication
1999
Pages
238 - 243
Database
ISI
SICI code
0001-6314(199910)100:4<238:AAISAC>2.0.ZU;2-Y
Abstract
Objectives - An autoimmune basis has been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS). This hypothesis is supported by the p resence of antibodies that interact with motoneuron antigens in serum of th ese patients. Against autoimmunity are the discrepances in the frequency of the antibodies appearance and also failure of immunosuppression. The aim o f our study was to evaluate the titer of antibodies against GM1-ganglioside s, AGM1-gangliosides and anti-sulfatides in paired serum and cerebrospinal fluid samples in the ALS patients. Materierl and methods - Serum of 103 and CSF of 79 patients with ALS was examined. The "disease controls" consisted of 22 cases of other motor neuron diseases and 50 healthy, age-matched nor mals. CSF was drawn at the same time from 79 ALS patients, 6 cases of the " disease controls" and 50 normals. To study the titer of antibodies against GM1-gangliosides, AGM1-gangliosides and sulfatides the ELISA technique has been applied. Results - An increased titer against GM1-gangliosides, AGM1-g angliosides and sulfatides in ALS appeared in serum in 18%, 32% and 11%, re sp., in the "disease controls" the increased antibodies titer appeared in s ingle cases. In CSF the appropriate values in ALS were 20%, 15%, 8%, resp. In the "disease controls" a high antibodies titer was a rare finding. Concl usions - It is concluded that in some ALS cases and also in some patients w ith other motor neuron diseases an autoimmune mechanism may contribute to m otor neuron injury.