Association of Amyloid Pathology With Myelin Alteration in Preclinical Alzheimer Disease

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Abstract
The progression of Alzheimer disease (AD) pathology occurs several years before the development of dementia. According to the amyloid-cascade hypothesis, the disruption of critical metabolic processes that lead to the ultimate neurodegeneration in AD is initiated by the accumulation of aggregated β-amyloid 1-42 (Aβ1-42) and the assembly of neurofibrillary tangles.1 Such processes are clearly detrimental to neuronal cell bodies, dendrites, and axonal processes; however, myelin and myelin-producing oligodendrocytes may be equally vulnerable to the impairments caused by Aβ and tau protein hyperphosphorylation.2 White matter hyperintensities (WMHs) play a role in symptom presentation but are not core features of AD pathology.3 Postmortem and in vivo magnetic resonance imaging (MRI) studies have substantiated recent hypotheses of white matter involvement in AD, finding reduced white matter volume and alterations of white matter microstructure.4-6 Still, little is known about the relationship between Aβ pathology and myelin alteration.

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