Author(s): Ewa Papuć and Konrad Rejdak
Although Alzheimer’s disease (AD) has been mainly considered as a grey matter disorder, there is emerging evidence that myelin impairment may play an important role in AD pathology. These data come from animal neuropathological studies, but also from human pathological, biochemical and brain MRI studies. Classical neuropathological changes in AD such as the accumulation of aggregated Aß 42 and the presence of neurofibrillary tangles are responsible for neuronall loss, but they may also induce death of oligodendrocytes and myelin impairment. Accelerated deposition of Aß in brains of AD patients induces damage to oligodendrocytes and results in impaired myelin production. What is more interesting, there is also evidence that myelin pathology may precede Aß and tau pathologies in AD. Recent studies suggest that Aß and tau proteins may be by-products of myelin repair in AD, instead of being the primary underlying cause of dementia. This seems possible, considering the fact that attempts to control clinical symtomps of AD by removing Aß from the human brain have been unsuccesful. In this article, current knowledge on the place of myelin in AD pathology and its interactions with Aß and tau pathology is reviewed.
