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The APOE4 isoform is a major genetic risk factor for late-onset AD, whereas APOE2 exerts a protective effect as explained earlier

These primary channelopathies (genetic component being in an ion channel gene) place a strain on energy metabolism, likely resulting in mitochondrial dysfunction, not only from the requirement to pump ions against the leak, but also from secondary effects on increased energy metabolism due to multiple aspects of cellular hyperexcitability