Dean, D., S. Hurley, S. Kecskemeti, J. O’Grady, C. Canda, N. Davenport-Sis, C. Carlsson, H. Zetterberg, K. Blennow, S. Asthana, M. Sager, S. Johnson, A. Alexander, and B. Bendlin. “Association of Amyloid Pathology With Myelin Alteration in Preclinical Alzheimer Disease.”. JAMA Neurology, Vol. 74, no. 1, 2017, pp. 41-49.
The accumulation of aggregated β-amyloid and tau proteins into plaques and tangles is a central feature of Alzheimer disease (AD). While plaque and tangle accumulation likely contributes to neuron and synapse loss, disease-related changes to oligodendrocytes and myelin are also suspected of playing a role in development of AD dementia. Still, to our knowledge, little is known about AD-related myelin changes, and even when present, they are often regarded as secondary to concomitant arteriosclerosis or related to aging.
DOI: 10.1001/jamaneurol.2016.3232
PubMed: 27842175