Boost glutamate receptors to restore synaptic function in FTD mice

  According to a study published in the Journal of Neuroscience, drugs that enhance the function of certain types of neurotransmitter receptors have a therapeutic effect in the second most common Alzheimer's disease (frontotemporal dementia). confirmed. Frontotemporal dementia, called FTD, is a devastating disease that causes major changes in the patient's behavior, personality, and social skills. The age of onset of FTD is relatively young, and the age of onset is in the late 1950s. The prognosis of the patient is severe, the condition deteriorates rapidly, and the patient usually dies within 10 years after the onset.

  The UAB research team is concerned about the mutations of certain genes, mainly the tau gene of the microtubule-associated protein. The accumulation of tau protein is associated with Alzheimer's disease (the most common form of Alzheimer's disease). However, few people know how mutations in the tau protein affect specific brain regions and cause FTD. UAB researchers are using a new mouse model that expresses mutations in the tau protein gene associated with FTD. These mice exhibited physical behaviors similar to those of FTD patients, including forced and excessive repetitive surgery, such as cosmetics. Certain areas of the mouse brain network have defective synapses and neural network functions. Erik Roberson, MD, said: We found that mutated tau protein disrupts synapses (connections between neurons) by reducing NMDA (glutamate receptors).

  Later, the research team used cycloserine, a drug approved by the FDA to enhance the function of NMDA receptors. The enhanced NMDA receptor function restores synaptic excitability, thereby enhancing neural network activity in animal models. I found that I can recover. Normal neural network activity can correct abnormal mouse behavior.

  This research helps us understand how mutations in tau protein affect specific brain regions and damage neural networks. It also provides potential therapeutic targets for NMDA receptors to correct network and behavior abnormalities. Obertson's research team speculates that increasing the function of NMDA receptors could benefit human FTD patients.