Primary research

Age‑related cognitive decline, including Alzheimer’s disease, can be understood as a myelin problem rather than only a “plaques and tangles” problem. Myelin is the fatty insulation around nerve fibres that makes brain signalling fast and efficient; in humans it continues to be built well into midlife, especially in frontal and temporal brain regions that support complex thinking. Because myelin is so metabolically expensive and turns over, it becomes increasingly vulnerable with age to oxidative damage, metabolic stress, and vascular insults, particularly in these late‑myelinating association areas.

As myelin gradually breaks down, signal transmission becomes noisy and inefficient, which shows up first as subtle cognitive changes and, when severe, contributes to the network failure seen in Alzheimer’s. Classical Alzheimer’s pathologies (amyloid, tau) are framed as interacting with and exacerbating this underlying myelin vulnerability rather than being the sole root cause. Overall, the model reframes Alzheimer’s as the late outcome of a lifelong, developmentally patterned process in which prolonged human myelination and later myelin breakdown are central.

Source: Neurobiology of Aging