Whether cause or effect, the extent of plaque and tangles generally increases as Alzheimer’s disease progresses. And tau protein tangles can appear to spread more actively once a level of amyloid beta plaques has developed.^13,22

One recent theory is that it may not necessarily be amyloid plaques building up that affects cognitive function, but is due to a relative lack of a specific protein, amyloid-beta 42. Research has found that a reduction in amyloid-beta 42 levels is associated with memory loss rather than the total number of plaques of insoluble amyloid beta. If amyloid-beta 42 levels are high, cognitive function is preserved. In addition, people with no plaques but who have low levels of amyloid-beta 42 can develop dementia.²⁷

Lecanemab and donamemab are new immunoglobulin IgG1 monoclonal antibodies targeting amyloid-beta plaques. Lecanemab prevents amyloid-beta depositing as plaques and appears to boost amyloid-beta 42 levels in cerebrospinal fluid, which may delay cognitive decline.^28,29