Increasing the level of an enzyme called EphB2 in nerve cells improves memory in mice suffering from Alzheimer’s, according to US scientists in the journal Nature. Their work suggests new goals for treating dementia.
Lennart Mucke of the Gladstone Institute of Neurological Disease and his team showed that mice with decreased levels of EphB2 kinase (an enzyme that attaches phosphate groups to other proteins) exhibit memory impairment similar to that of humans with Alzheimer’s.
Rodents have a disturbed mechanism of the so-called long-term synaptic arousal (LTP) – a sequence of electrical changes underlying learning and memory, and changes in the functioning of glutamate neurotransmitter receptors, key to cognitive processes.
Scientists have shown that fragments of beta amyloid, responsible for the formation of senile plaques in the brains of Alzheimer’s patients, bind to the EphB2 enzyme and cause its degradation.
According to the authors of the study, drugs that increase the level of EphB2 kinase may prove to be effective in the treatment of Alzheimer’s disease, as well as molecules that prevent the binding of amyloid beta to EphB2 and prevent its degradation. (PAP)