Health
Researchers Identify Enzyme as Potential Target to Slow Alzheimer’s Memory Loss
Scientists have identified a potential new approach to slow memory loss in Alzheimer’s disease, offering hope for treatments that could improve the lives of millions affected by the neurodegenerative disorder.
Researchers at Cold Spring Harbor Laboratory, a non-profit research institution in New York, found that an enzyme called PTP1B contributes to memory decline in mice with Alzheimer’s. The study reveals a previously unknown role for the enzyme in immune cell signaling and suggests it could be a promising target for therapy.
Nicholas Tonks, a professor at the laboratory and the study’s corresponding author, discovered PTP1B in 1988 and has since explored its role in health and disease. Tonks and his team found that reducing PTP1B activity improved the ability of the brain’s immune cells, known as microglia, to clear amyloid-β (Aβ) plaques. These protein accumulations are a hallmark of Alzheimer’s disease and contribute to neuronal damage. Normally, microglia remove debris in the brain, but their function declines as the disease progresses.
The researchers discovered that PTP1B interacts with a protein called spleen tyrosine kinase (SYK), which regulates microglial responses to damage and plaque clearance.
“Over the course of the disease, these cells become exhausted and less effective,” said Yuxin Cen, the study lead. “Our results suggest that PTP1B inhibition can improve microglial function, clearing up Aβ plaques.”
PTP1B is also known for its role in metabolic conditions such as obesity and type 2 diabetes, which are recognized risk factors for Alzheimer’s disease. Researchers are now working to develop PTP1B inhibitors for multiple applications, including as a potential therapy for the neurodegenerative condition.
Tonks envisions combining PTP1B inhibitors with existing approved drugs for Alzheimer’s, such as cholinesterase inhibitors like donepezil or NMDA receptor antagonists such as memantine, used for more advanced stages.
“The goal is to slow Alzheimer’s progression and improve the quality of life of the patients,” Tonks said. He added that the research is particularly personal: “It’s a slow bereavement. You lose the person piece by piece,” recalling his mother’s experience with the disease.
According to the World Health Organization, more than 55 million people live with dementia globally, with Alzheimer’s accounting for up to 70 percent of cases. Current treatments manage symptoms but do not halt disease progression, making the search for new therapies critical.
The Cold Spring Harbor Laboratory team says their findings open the door to a new pathway for treatment, targeting the immune system’s capacity to remove harmful plaques. Researchers are hopeful that continued development of PTP1B inhibitors could complement existing drugs and slow the devastating effects of Alzheimer’s, potentially transforming care for millions worldwide.
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