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Портал Begell Электронная Бибилиотека e-Книги Журналы Справочники и Сборники статей Коллекции
Critical Reviews™ in Neurobiology
SJR: 0.121

ISSN Печать: 0892-0915
ISSN Онлайн: 2375-0014

Archives: Volume 10, 1996 to Volume 20, 2008

Critical Reviews™ in Neurobiology

DOI: 10.1615/CritRevNeurobiol.v16.i12.150
pages 141-146

Peripheral Markers of Glutamatergic Dysfunction in Neurological Diseases: Focus on Ex Vivo Tools

Lucio Tremolizzo
The Psychiatric Institute, Department of Psychiatry, University of Illinois at Chicago, Chicago Illinois, USA
Simone Beretta
Department of Neurology, S. Gerardo Hospital and Department of Neuroscience and Biomedical Technologies, University of Milano-Bicocca, Monza, Italy
Carlo Ferrarese
Department of Neurology, S. Gerardo Hospital and Department of Neuroscience and Biomedical Technologies, University of Milano-Bicocca, Monza, Italy

Краткое описание

Since the proposal that excessive glutamatergic stimulation could be responsible for neuronal suffering and death, excitotoxicity and glutamate uptake deficits have been repeatedly confirmed to play a key role in the pathogenesis of different neurological diseases. Therefore, it is conceivable that assessing the glutamatergic system function directly in patients could be extremely useful for early diagnosis, prognostic evaluation, and optimization of the therapy. A possibility is offered by assessing glutamate levels in biological fluid, such as plasma and CSF, where increased levels of this amino acid have been reported in patients affected by stroke, amyotrophic lateral sclerosis (ALS), and AIDS dementia complex. However, the metabolic role of this amino acid acts as a confounding factor, and the possibility of directly assessing glutamatergic functional parameters, such as amino acid reuptake, would probably mirror closely the actual excitotoxic damage operative in each patient. Here we will describe our findings obtained in peripheral ex vivo cells, such as platelets and fibroblasts, both displaying a functional glutamate reuptake system. Consistent with a systemic-impairment assumption, glutamate uptake was shown to be reduced in peripheral cells of Alzheimer's disease, Down syndrome, Parkinson's disease, ALS, and stroke patients. Different systemic factors might be responsible for this phenomenon, including genetic predisposition, oxidative stress, and inflammatory response, raising new, exciting questions about the relevance of their possible interactions for the pathogenesis of neurological disorders.

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