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Abstract
Accumulating evidence has revealed that immunity plays an important role in amyotrophic lateral sclerosis (ALS) progression. However, the results regarding the serum levels of immunoglobulin and complement are inconsistent in patients with ALS. Although immune dysfunctions have also been reported in patients with other neurodegenerative diseases, few studies have explored whether immune dysfunction in ALS is similar to that in other neurodegenerative diseases. Therefore, we performed this study to address these gaps. In the present study, serum levels of immunoglobulin and complement were measured in 245 patients with ALS, 65 patients with multiple system atrophy (MSA), 60 patients with Parkinson's disease (PD), and 82 healthy controls (HCs). Multiple comparisons revealed that no significant differences existed between patients with ALS and other neurodegenerative diseases in immunoglobulin and complement levels. Meta-analysis based on data from our cohort and eight published articles was performed to evaluate the serum immunoglobulin and complement between patients with ALS and HCs. The pooled results showed that patients with ALS had higher C4 levels than HCs. In addition, we found that the IgG levels were lower in early-onset ALS patients than in late-onset ALS patients and HCs, and the correlations between age at onset of ALS and IgG or IgA levels were significant positive. In conclusion, our data supplement existing literature on understanding the role of peripheral immunity in ALS.
Highlights
Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease characterized by the progressive degeneration of upper and lower motor neurons at the motor cortex, bulbar, and spinal levels, leading to muscle weakness, progressive paralysis, and respiratory failure and death within 3–5 years after disease onset [1]
There were no significant differences in the levels of IgA, IgM, or C4 among the patients with amyotrophic lateral sclerosis (ALS), multiple system atrophy (MSA), and Parkinson’s disease (PD) and healthy controls (HCs) (Table 2 and Figure 1)
No significant differences in serum C3 levels were found between the ALS patients and HCs, PD patients and HCs, ALS patients and MSA patients, or ALS patients and MSA patients
Summary
Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease characterized by the progressive degeneration of upper and lower motor neurons at the motor cortex, bulbar, and spinal levels, leading to muscle weakness, progressive paralysis, and respiratory failure and death within 3–5 years after disease onset [1]. The activation of astrocytes and microglia and the infiltration of T cells and monocytes have been observed in the central nervous system (CNS) of patients with ALS and animal models [5,6,7,8]. Increased levels of complement C3 and C5a, C reactive protein (CRP), and erythrocyte sedimentation rate (ESR) as well as T cell abnormalities and immunoglobulin alterations were found in the blood of patients with ALS [16, 18,19,20,21,22]. There is strong evidence of complement upregulation in ALS, normal C3 and C4 levels were observed in patients with ALS [25, 28], and the specific genetic deletion of C3 and C4 in ALS mouse models did not show any beneficial effects on the disease progression [12, 29]
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