Decreased levels of soluble amyloid β-protein precursor and β-amyloid protein in cerebrospinal fluid of patients with systemic lupus erythematosus

Arthritis Research & Therapy

Andrej Tarkowski²  Kaj Blennow¹  Elisabet Svenungsson³  Kina Höglund¹  Estelle Trysberg² 

[1]Institute of Clinical Neuroscience, Göteborg University, Sahlgrenska University Hospital, Göteborg, Sweden

[2]Department of Rheumatology and Inflammation Research, Göteborg University, Sahlgrenska University Hospital, Göteborg, Sweden

[3]Department of Rheumatology and Center for Molecular Medicine, Karolinska Hospital, Stockholm, Sweden

关键词: tau;    neuropsychiatric systemic lupus erythematosus;    cerebrospinal fluid;    β-amyloid protein;    amyloid precursor protein;   

Others  :  1101298
DOI  :  10.1186/ar1040

 received in 2003-11-24, accepted in 2004-01-07,  发布年份 2004

【 摘 要 】

Symptoms originating from the central nervous system (CNS) frequently occur in patients with systemic lupus erythematosus (SLE). These symptoms are extremely diverse, including a state of dementia. The aim of this study was to examine the cerebrospinal fluid (CSF) content of soluble molecules indicating axonal degeneration and amyloidogenesis.

One hundred and fourteen patients with SLE and age-matched controls were evaluated clinically, with magnetic resonance imaging of the brain and CSF analyses. Levels of tau, amyloid precursor protein (APP), β-amyloid protein (Aβ42), and transforming growth factor beta (TGF-β) were all determined using sandwich ELISAs.

APP and Aβ42 levels were significantly decreased in SLE patients irrespective of their CNS involvement, as compared with healthy controls. Patients with neuropsychiatric SLE who underwent a second lumbar puncture following successful cyclophosphamide treatment showed further decreases of Aβ42. CSF-tau levels were significantly increased in SLE patients showing magnetic resonance imaging-verified brain pathology as compared with SLE patients without such engagement. Importantly, tau levels displayed significant correlation to Aβ42 levels in the CSF. Finally, TGF-β levels were significantly increased in patients with neuropsychiatric SLE as compared with those without.

Low intrathecal levels of Aβ42 found in SLE patients seem to be a direct consequence of a diminished production of APP, probably mediated by heavy anti-inflammatory/immuno-suppressive therapy. Furthermore, our findings suggest that CSF tau can be used as a biochemical marker for neuronal degeneration in SLE. Finally, the increased TGF-β levels observed may support a notion of an ongoing anti-inflammatory response counteracting tissue injury caused by CNS lupus.

【 授权许可】

   
2004 Trysberg et al., licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.

【 图 表 】

Figure 2.

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