Demyelination Accelerates Amyloid- β Aggregation

Nerves require myelin sheathing in order to function correctly. With age, some degree of dysfunction in myelin maintenance takes place, with consequent cognitive and other nervous system degeneration as a consequence. This loss of myelin integrity takes place to a lesser degree than is the case in severe demyelinating conditions such as multiple sclerosis. Nonetheless, that lesser degree may be contributing to the early stages of Alzheimer's disease by reducing immune clearance of amyloid-β aggregates. At present a question hovers over the role of amyloid-β in Alzheimer's disease due to the failure of amyloid-clearing immunotherapies to improve patient outcomes in the clinic. The research and development communities remain largely wedded to the idea that amyloid-β aggregation will turn out to be relevant to the early onset of the condition, but it remains to be seen as to whether even that is correct, accepting that the later stages have moved on to other primary mechanisms of harm associated with neuroinflammation and tau aggregation. Poorly insulated nerve cells promote Alzheimer's disease in old age Intact myelin is critical for normal brain function. Researchers have shown that age-related changes in myelin promote pathological changes in Alzheimer's disease. Their work focused on a typical feature of the disease; Alzheimer's is characterized by the deposition of certain proteins in the brain, the so-called amyloid beta peptides (Aβ). The Aβ pe...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs