Defective cerebral gamma-aminobutyric acid-A receptor density in patients with systemic lupus erythematosus and central nervous system involvement. An observational study

Author:

Mathieu A.1,Vacca A.2,Serra A.3,Cauli A.2,Piga M.2,Porru G.2,Marrosu F.4,Sanna G.5,Piga M.3

Affiliation:

1. Chair and AOU Unit of Rheumatology, University of Cagliari, Italy,

2. Chair and AOU Unit of Rheumatology, University of Cagliari, Italy

3. Chair and AOU Unit of Nuclear Medicine, University of Cagliari, Italy

4. Department of Neurological and Cardiovascular Sciences, University of Cagliari, Italy

5. Lupus Research Unit The Rayne Institute, St Thomas' Hospital, London, UK

Abstract

Gamma-aminobutyric acid-A (GABA-A) receptors play a crucial role in regulating neuronal excitability and cognitive functions. Single-photon emission computerized tomography (SPECT) analysis of GABA-A receptors binding by 123I-labelled Iomazenil (123I-IMZ) has been applied in some neuropsychiatric disorders to investigate conditions where GABA-A receptor density can be detected in several pathophysiological conditions. In this study we investigate cerebral GABA-A receptor density in a small series of patients with systemic lupus erythematosus (SLE) and cognitive impairment characterized by recurrent, episodic memory loss. Nine female patients with SLE and cognitive alterations underwent to a clinical neuropsychiatric evaluation including digital video-EEG, brain MRI, 99mTc-ECD brain SPECT and 123I-IMZ brain SPECT. All patients tested showed diffuse or focal GABA-A receptor density reduction. This is, to our knowledge, the first report on GABA-A receptor density abnormalities associated with cognitive defects in SLE patients. We hypothesize that in our series a decrease in GABA-A receptor density might be related to the neurological manifestations. Further studies are needed to clarify this aspect and the possible mechanisms. GABA-A receptor density impairment might be due to the SLE-related cerebral vasculopathy, or to neuronal-reacting auto-antibodies or drugs which could interfere with GABA-A receptors expression/binding. This study may support the concept that cognitive impairment in systemic lupus erythematosus could be the outcome of fine-tuned neurotransmission alterations.

Publisher

SAGE Publications

Subject

Rheumatology

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