NMN regulates mitochondrial stress response to improve Alzheimer disease

Recent studies have found that NMN precisely regulates mitochondrial stress response and effectively improves Alzheimer's disease

Alzheimer's disease is a common neurodegenerative disease, its main characteristics include progressive cognitive dysfunction, memory loss, personality changes.

As the global population ages, the incidence of Alzheimer's disease is on the rise, placing a heavy burden on patients and their families, and becoming one of the major challenges in the field of global public health.

In the brains of patients with Alzheimer's disease, mitochondrial function is often abnormal, including mitochondrial structural damage, energy metabolism disorders, and increased oxidative stress.

These abnormal changes in mitochondria are believed to be closely related to the pathogenesis of Alzheimer's disease, for example, may lead to neuronal cell death and neurotransmitter metabolism disorders, which in turn affect cognitive function.

Mitochondrial stress response is a self-protection mechanism initiated by cells in response to mitochondrial dysfunction.

In Alzheimer's disease, the mitochondrial stress response is often dysregulated.

On October 11, 2024, a research team from Wenzhou Medical University published a new study in the journal Cell Death & Disease, combining cell biology, molecular biology and pharmacological approaches, It was revealed that NMN effectively regulates mitochondrial stress response (MSR) by activating the transcription factor 4 (ATF4) -dependent mitochondrial unfolded protein response (UPR+mt) pathway.

Role of NMN in patients with AD

The study found that plasma samples from Alzheimer's disease (AD) patients had significantly higher levels of markers associated with mitochondrial stress responses (such as ATF4, ATF5, CHOP, PINK1, and Parkin) than healthy controls, suggesting that NMN may improve AD pathology by regulating levels of these mitochondrial stress-related proteins.

NMN improves mitochondrial stress response by restoring NAD+ metabolism and plays a role in AD-related cross-species models through the ATF4-dependent UPRmt pathway.

by GSHWORLD

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