黑料吃瓜资源

Alzheimer鈥檚 disease is often measured in statistics: millions affected worldwide, cases rising sharply, costs climbing into the trillions. For families, the disease is experienced far more intimately. 鈥淚t鈥檚 a slow bereavement,鈥� says 黑料吃瓜资源 Professor Nicholas Tonks, whose mother lived with Alzheimer鈥檚. 鈥淵ou lose the person piece by piece.鈥�

There鈥檚 a lot of discussion about how the neurodegenerative disorder may be caused by a buildup of 鈥減laque鈥� in the brain. When someone refers to this plaque, they鈥檙e talking about amyloid-尾 (A尾), a peptide that occurs naturally but can accumulate and come together. This is known to promote Alzheimer鈥檚 disease development.

Now, Tonks, graduate student Yuxin Cen, and postdoctoral fellow Steven Ribeiro Alves have discovered that inhibiting a protein called PTP1B improves learning and memory in an Alzheimer鈥檚 disease mouse model.

Tonks discovered in 1988 and has studied this enzyme鈥檚 implications for health and disease ever since. In this latest study, his team shows how PTP1B directly interacts with another protein called spleen tyrosine kinase (SYK), which normally regulates microglia (the brain鈥檚 immune cells) to clear out debris like excess A尾. 鈥淥ver the course of the disease, these cells become exhausted and less effective,鈥� says Cen. 鈥淥ur results suggest that PTP1B inhibition can improve microglial function, clearing up A尾 plaques.鈥�

Beyond A尾, obesity and type 2 diabetes are well recognized risk factors for Alzheimer鈥檚 disease and are believed to contribute to its increasing prevalence worldwide. These links provide additional rationale for going after PTP1B in Alzheimer鈥檚 disease, as it鈥檚 a validated therapeutic target for both metabolic disorders.

Newly approved therapies for Alzheimer鈥檚 disease primarily focus on targeting A尾 clearance, yet offer only modest clinical benefits for many patients. 鈥淯sing PTP1B inhibitors that target multiple aspects of the pathology, including A尾 clearance, might provide an additional impact,鈥� says Ribeiro Alves.

The Tonks lab is currently working with DepYmed, Inc. to develop PTP1B inhibitors for multiple applications. For Alzheimer鈥檚 disease, Tonks envisions a combination of therapies that pair existing approved drugs along with PTP1B inhibitors. 鈥淭丑别 goal is to slow Alzheimer鈥檚 progression and improve quality of life of the patients,鈥� he says. With this research establishing PTP1B as a potential therapeutic target for the disease, it may hold the key to doing just that.

Written by: Gina DiPietro, Senior Public Relations Specialist | [email protected] | 516-367-6826

Funding

National Institutes of Health, 黑料吃瓜资源, Coins for Alzheimer鈥檚 Research Trust, Hansen Foundation; compounds provided by DepYmed Inc.

Citation

Cen, Y., et al., 鈥淧TP1B inhibition promotes microglial phagocytosis in Alzheimer鈥檚 disease models by enhancing SYK signaling鈥�, Proceedings of the National Academy of Sciences, February 2, 2026. DOI:

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