Myelin dysfunction drives amyloid-β deposition in models of Alzheimer’s disease
Max Planck Institute of Experimental Medicine · Max Planck Institute for Multidisciplinary Sciences · +9 more institutions
Abstract
Abstract The incidence of Alzheimer’s disease (AD), the leading cause of dementia, increases rapidly with age, but why age constitutes the main risk factor is still poorly understood. Brain ageing affects oligodendrocytes and the structural integrity of myelin sheaths 1 , the latter of which is associated with secondary neuroinflammation 2,3 . As oligodendrocytes support axonal energy metabolism and neuronal health 4–7 , we hypothesized that loss of myelin integrity could be an upstream risk factor for neuronal amyloid-β (Aβ) deposition, the central neuropathological hallmark of AD. Here we identify genetic pathways of myelin dysfunction and demyelinating injuries as potent drivers of amyloid deposition in…
Citation impact
- FWCI
- 47.21
- Percentile
- 100%
- References
- 88
Authors
30- CDConstanze DeppCorresponding
Max Planck Institute of Experimental Medicine, Max Planck Institute for Multidisciplinary Sciences
- TSTing Sun
Max Planck Institute for Multidisciplinary Sciences
- AOAndrew Octavian Sasmita
Max Planck Institute for Multidisciplinary Sciences
- LSLena Spieth
German Center for Neurodegenerative Diseases, Max Planck Institute for Multidisciplinary Sciences
- SAStefan A. Berghoff
German Center for Neurodegenerative Diseases, Max Planck Institute for Multidisciplinary Sciences
Topics & keywords
- Myelin
- Microglia
- Oligodendrocyte
- Amyloid (mycology)
- Amyloid precursor protein
- Neuroscience
- Amyloid beta
- Biology