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Apolipoprotein E ablation decreases synaptic vesicular zinc in the brain
Joo-Yong Lee1, Eunsil Cho, Tae-Youn Kim
1Asan Institute for Life Sciences, Asan Medical Center, Seoul, 138-736, Republic of Korea.
Summary
Apolipoprotein E (apoE) deficiency reduces synaptic zinc levels in mouse brains, impacting Alzheimer's disease (AD) pathology. This suggests apoE influences cerebral zinc, a factor in AD.
Area of Science:
- Neuroscience
- Biochemistry
- Pathology
Background:
- Apolipoprotein E (apoE) and zinc are implicated in Alzheimer's disease (AD) neuropathology, specifically amyloid-beta (Aβ) aggregation.
- Interactions between apoE and metal ions may accelerate brain amyloidogenesis.
Purpose of the Study:
- To investigate the impact of apoE deficiency on the histochemically reactive zinc pool in the brains of apoE knockout mice.
- To understand the role of apoE in regulating cerebral zinc levels relevant to AD.
Main Methods:
- Comparison of zinc levels in apoE-deficient mice versus wild-type mice.
- Analysis of metal content (zinc, copper, iron) and histochemically reactive zinc.
- Assessment of presynaptic zinc transporter (ZnT3) and AP3δ subunit expression.
Main Results:
- ApoE deficiency significantly reduced histochemically reactive (synaptic) zinc levels without altering total metal content.
- Reduced expression of ZnT3 and AP3δ was observed in apoE-deficient brains.
- Histochemically reactive zinc was also decreased in cerebrovascular micro-vessels of apoE-deficient mice.
Conclusions:
- Apolipoprotein E influences the cerebral free zinc pool, particularly synaptic zinc.
- Reduced zinc levels and altered ZnT3/AP3δ expression in apoE-deficient mice suggest a mechanism linking apoE to AD-related zinc dysregulation.
- These findings highlight a potential role for apoE in modulating zinc's contribution to Alzheimer's disease pathology.
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