Clinical Neuroscience

[Regulation of water transport in brain oedema]

DÓCZI Tamás, SCHWARCZ Attila, GALLYAS Ferenc, BOGNER Péter, PÁL József, SULYOK Endre, GÖMÖRI Éva, VAJDA Zsolt

OCTOBER 10, 2005

Clinical Neuroscience - 2005;58(09-10)

[The study gives an overview on the regulation of cerebral water content and of brain volume. The molecular mechanisms of the development and resolution of various oedema forms are discussed in detail. The physiological and pathophysiological role of the recently discovered molecular water channel proteins aquaporin-1 (AQP1) and aquaporin-4 (AQP4) as well as the importance of central neuroendocrine regulation by vasopressin and atriopeptin are reviewed based on the relevant literature and personal studies. Quantitative water maps based on the combination of multicompartment- T2, diffusion weighted MRI and T1 studies have proven to be powerful tools for studying new drugs against brain oedema brought about by various neuropathological conditions and for testing their efficacy both in animal experimental and clinical conditions. Non-peptide vasopressin antagonists, atriopeptin agonists and drugs targeting AQP4 are potential new families of oedema-decreasing drugs.]



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[Stroke-related death is the third most common cause of mortality in Hungary after cardiovascular diseases and cancer. In addition to the unfavourable mortality figures, the consequent development of neurological and psychiatric disorders in stroke patients imposes an enormous burden on the health care system and on the families. Numerous studies are being conducted world wide on the prevention of stroke and other cerebrovascular disorders like chronic hypoperfusion, as well as on acute stroke management and patient rehabilitation issues. As a result, our understanding of the mechanism of hypoxic brain damage steadily increased over the past years and decades which brought along promising achievements both in the field of stroke prevention and therapy. However, these broad-spectrum approaches also made clear that preventing neuronal death and thus reducing neurological damage are complex tasks that cannot be successfully resolved by targeting single mechanisms. Therefore, the development of alternative new drugs and clinically applicable complex neuroprotective strategies is warranted. One of the most promising approaches is to create ischemic tolerance in the brain by using pharmacological preconditioning paradigms. These drugs trigger similar events to those initiated by brief ischemic insults that later can make the cerebral tissue resistant to subsequent otherwise lethal stress (ischemic preco]

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Clinical Neuroscience



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