Publication: Disruption of brain zinc homeostasis promotes the pathophysiological progress of Alzheimer's disease
Authors
Li, Lin-Bo ; Wang, Zhan-You
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Publisher
Universidad de Murcia. Departamento de Biología Celular e Histología
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DOI
DOI: 10.14670/HH-11-737
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info:eu-repo/semantics/article
Description
Abstract
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.
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Citation
Histology and histopathology: Vol.31, nº6 (2016)
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