Behavior of neural networks in culture suggest that sporadic and genetic forms of Alzheimer's disease may not be equivalent

Description

Fulin Ma, Himanshu Akolkar, Ryad Benosman, and Karl Herrup question a common assumption in Alzheimer's research: that the inherited and sporadic forms of the disease are basically the same. The two forms involve the amyloid precursor protein in different ways. In one, mutations change the protein; in the other, age brings too much of it or deposits of amyloid beta. The team compared these routes in cultured neurons.

Using dense electrode arrays, they tracked firing, synapse formation, branch growth, and network links in young and mature cultures. Extra precursor protein lowered firing odds and hurt synapse formation and branching during development. Amyloid beta, by contrast, broke synapses in mature cultures and weakened network communication without blocking early growth. The authors argue the two insults act through different paths. That difference, they say, should make researchers cautious about treating the two disease forms as one.

Catalog record

Source: https://europepmc.org/articles/PMC13240566