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Alzheimer's-linked apolipoprotein E produced by neurons, Gladstone study

underlying apoE4-related neurodegenerative disorders.’

‘ApoE expression can be detected with unprecedented sensitivity and resolution in these mice,’ explains Qin Xu, PhD, a Gladstone postdoctoral scholar and first author of the paper. ‘This mouse model, known as the 'EGFP knock-in,' is a new and extremely promising approach to monitor gene expression in vivo.’ ‘Our EGFPapoE reporter mice can be used to track apoE expression in any tissue at any stage of development,’ adds Huang. ‘They will be a valuable tool for investigating the normal functions of apoE and the regulatory mechanisms that govern its expression.’

Still to be determined is the exact mechanism by which apoE4 wreaks havoc on the brain, playing roles not only in Alzheimer's disease but also in a number of other neurological diseases. Studies in Huang's lab have revealed a possible scenario. It appears that apoE in neurons is subject to processing by an enzyme that clips off a portion of the protein, resulting in toxic fragments that escape the secretory pathway and enter the cytosol (the fluid portion of a cell's cytoplasm). Studies now underway at Gladstone and elsewhere indicate that those fragments may interfere with glucose metabolism in the mitochondria (small intracellular organelles responsible for energy production, among other functions), leading to mitochondrial dysfunction and neuronal cell death.

The paper, ‘Profile and Regulation of Apolipoprotein (Apo) E Expression in Central Nervous System in Mice with Targeting of Green Fluorescent Protein Gene to the apoE Locus,’ was authored by Aubrey Bernardo, David Walker, and Tiffany Kanegawa of the Gladstone Institute of Neurological Disease, Gladstone Institutes President Robert W. Mahley, and Xu and Huang. This work was supported in part by grants from the National Institutes of Heath and a postdoctoral fellowship from the John Douglas French Alzheimer's Foundation.

Soure: Eurekalert
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