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Modification of CKB is associated with β-amyloid depositions and a loss of function of APOE as a scavenger for lipid peroxidation-derived aldehydes 202 as both APOE deletion 203 and high levels of lipid peroxidation products are associated with increased lipoxidative modifications of CKB, GS, vimentin and GFAP 204

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Atrophy of hypothenar eminence and interosseous muscles is also a frequently reported symptom [21,22]

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