Neuroscientist Luísa Lopes, a researcher at GIMM, was invited by the journal Cell to comment on a new study that may change the way we understand Alzheimer’s disease1.
For many years, scientists focused on a protein called beta-amyloid as the major cause of memory dysfunction and other cognitive difficulties associated with Alzheimer’s. But the new study points in a different direction: another protein, called tau (in its soluble and harder-to-detect form), may be the main factor disrupting neuronal firing in the early stages of the disease1.
In her commentary, co-authored with Paula Pousinha2, Lopes explains that this form of tau interferes with “burst firing” in neurons, a process critical for memory. The findings suggest that targeting soluble forms of tau early – before it forms tangles – could be key to preventing memory loss. And by using brain samples from patients, the study makes a strong case for therapies that focus beyond beta-amyloid.
1Harris, S.S., Ellingford, R., Hartmann, J., Das- gupta, D., Kehring, M., Rajani, R.M., Graykow- ski, D., Quittot, N., Sivasankaran, D., Com- mins, C., et al. (2025). Alzheimer’s disease patient-derived high-molecular-weight tau impairs bursting in hippocampal neurons. Cell 188, 3775-3788
2 Lopes and Pousinha, Burst firing in Alzheimer’s disease: A shift beyond amyloid?, Cell (2025), DOI: 10.1016/j.cell.2025.06.016