Defective cerebral gamma-aminobutyric acid-A receptor density in patients with systemic lupus erythematosus and central nervous system involvement. An observational study
Autor: | A. Mathieu, A. Vacca, A. Serra, A. Cauli, M. Piga, G. Porru, F. Marrosu, G. Sanna |
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Rok vydání: | 2010 |
Předmět: |
Adult
Central Nervous System Flumazenil Pathology medicine.medical_specialty Central nervous system Neurotransmission Electroencephalography gamma-Aminobutyric acid Iodine Radioisotopes Rheumatology Pregnancy medicine Humans Lupus Erythematosus Systemic Receptor Cerebral Cortex Tomography Emission-Computed Single-Photon Iomazenil Lupus erythematosus medicine.diagnostic_test GABAA receptor business.industry Middle Aged medicine.disease Receptors GABA-A Magnetic Resonance Imaging medicine.anatomical_structure Cerebrovascular Circulation Female Radiopharmaceuticals business Cognition Disorders medicine.drug |
Zdroj: | Lupus. 19(8) |
ISSN: | 1477-0962 |
Popis: | 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. |
Databáze: | OpenAIRE |
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