PNAS: Blocking the protein PTP1B slows memory decline in Alzheimer's disease.
Scientists from the Cold Spring Harbor Laboratory in the USA have discovered that blocking the protein PTP1B may slow the decline of memory and learning in Alzheimer's disease. Experiments on mice showed that when this enzyme is suppressed, brain immune cells begin to more effectively clear toxic amyloid plaques — one of the key hallmarks of the disease. The results of the study are published in the Proceedings of the National Academy of Sciences (PNAS).
PTP1B has long been known to scientists as a protein associated with metabolism and conditions such as obesity and type 2 diabetes. The new study found that it also interferes with the normal functioning of microglia — the brain's immune cells. These cells are responsible for the 'clean-up' of amyloid, but as Alzheimer's disease progresses, they become depleted and lose effectiveness. Blocking PTP1B restores their activity and enhances the brain's clearance of harmful deposits.
It is also important that PTP1B interacts with the protein SYK, which directly regulates the function of microglia. Targeting this mechanism improved cognitive functions in animals with an Alzheimer's disease model — they performed better on memory and learning tasks. According to the authors, this indicates a fundamentally new approach to therapy that addresses not just one, but several processes associated with the disease.
Researchers emphasize that PTP1B is already being considered as a drug target for metabolic disorders. In the future, such inhibitors could be used alongside already approved medications to slow disease progression and maintain patients' quality of life for longer.
