Postmortem, RNA sequencing has revealed three major molecular subtypes of [Alzheimer’s] disease, each of which presents differently in the brain and which holds a unique genetic risk.
Such knowledge could help us predict who is most vulnerable to each subtype, how their disease might progress and what treatments might suit them best, potentially leading to better outcomes.
It could also help explain why effective treatments for AD have proved so challenging to find thus far.
Typically, accumulations of Aβ, [amyloid-beta plaques,] and NFT, [tau protein tangles,] are thought to drive neuronal and synaptic loss, predominantly within the cerebral cortex and hippocampus. Further degeneration then follows, including inflammation and degeneration of nerve cells’ protective coating, which causes signals in our brains to slow down.
Strangely enough, however, recent evidence has shown up to a third of patients with a confirmed, clinical diagnosis have no Aβ plaques in postmortem biopsies. What’s more, many of those found with plaques at death did not show cognitive impairment in life.
In light of all this research, it’s highly likely there are specific subtypes of AD that we simply haven’t teased apart yet. The new research has helped unbraid three major strands.