In a breakthrough that could transform Alzheimer's treatment, scientists at Karolinska Institutet in Sweden and the RIKEN Center for Brain Science in Japan have identified two brain receptors that help regulate the breakdown of amyloid beta — the protein that builds up as plaques in the brains of Alzheimer's patients.
The findings, published in the Journal of Alzheimer's Disease, suggest it may be possible to develop future medications that are both safer and more affordable than today's antibody-based treatments.
How the Brain Fights Back
Normally, an enzyme called neprilysin helps clear away amyloid beta (Aβ). However, neprilysin activity declines with aging and as the disease progresses. The research team discovered that two somatostatin receptors — SST1 and SST4 — work together to control neprilysin levels in the hippocampus, the brain region essential for memory.
When both receptors were missing in genetically modified mice, neprilysin levels dropped dramatically. As a result, amyloid beta accumulated and the mice showed memory problems.
A New Path to Treatment
The team tested a compound designed to activate these two receptors. In mice with Alzheimer's-like brain changes, stimulating SST1 and SST4:
- ✅ Increased neprilysin levels
- ✅ Reduced amyloid beta buildup
- ✅ Improved behavior and memory
- ✅ Caused no serious side effects
"Our findings show that the brain's own defence against amyloid beta can be strengthened by stimulating these receptors," says Per Nilsson, docent at Karolinska Institutet.
Why This Matters
Current antibody-based Alzheimer's therapies are extremely expensive and can trigger significant side effects. If researchers can develop small molecules that cross the blood-brain barrier to activate these receptors, it could mean dramatically cheaper treatments with fewer risks — bringing hope to the 55 million people worldwide living with dementia.
Source: Karolinska Institutet / Journal of Alzheimer's Disease, February 2026