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DOI: 10.14670/HH-11-737
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Título: | Disruption of brain zinc homeostasis promotes the pathophysiological progress of Alzheimer's disease |
Fecha de publicación: | 2016 |
Editorial: | Universidad de Murcia. Departamento de Biología Celular e Histología |
Cita bibliográfica: | Histology and histopathology: Vol.31, nº6 (2016) |
ISSN: | 1699-5848 0213-3911 |
Materias relacionadas: | CDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncología |
Palabras clave: | Alzheimer’s disease Divalent metal transporter Metal chelator Zinc Zinc transporte |
Resumen: | Zinc is abundant in the brain, where it plays an important role in synaptic plasticity and in learning; however, excessive zinc is toxic to neuronal cells, and dyshomeostasis of zinc in the brain is a contributing factor for Alzheimer’s disease (AD). Deposition of zinc has been detected in senile plaques in the form of zincAβ (β-amyloid) complexes. Recent studies have demonstrated that zinc exposure to the brain enhances βamyloid precursor protein (APP) expression, amyloidogenic APP cleavage and plaque burden. Furthermore, alterations in zinc transporters, which are responsible for zinc homeostasis, occur in AD human brain and transgenic mouse models. These suggest that abnormal brain zinc homeostasis is involved in the pathophysiological progress of AD. |
Autor/es principal/es: | Li, Lin-Bo Wang, Zhan-You |
URI: | http://hdl.handle.net/10201/111282 |
DOI: | DOI: 10.14670/HH-11-737 |
Tipo de documento: | info:eu-repo/semantics/article |
Número páginas / Extensión: | 5 |
Derechos: | info:eu-repo/semantics/openAccess Attribution-NonCommercial-NoDerivatives 4.0 Internacional |
Aparece en las colecciones: | Vol.31, nº6 (2016) |
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Li-31-623-627-2016.pdf | 170,68 kB | Adobe PDF | Visualizar/Abrir |
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