Protective Brain Protein Emerges as Biomarker Target in Alzheimer’s Disease
Posted on 27 Feb 2026
Alzheimer’s disease affects millions worldwide and still lacks effective therapies that halt or reverse its progression, underscoring the need for earlier insight into its molecular drivers and clinically practical biomarkers. Addressing this gap, investigators in Norway are focusing on a protective neuronal protein that appears reduced in individuals with Alzheimer’s disease and declines further as the condition advances. New findings indicate that modulating this target in disease models, while monitoring its levels in patients, may help inform therapeutic strategies and support biomarker development.
A team led by researchers at the University of Oslo and Akershus University Hospital identified the REST protein as a protective factor essential for neuronal resilience and proper function. Individuals with Alzheimer’s disease reportedly showed significantly lower REST levels than healthy older adults, with further declines observed as the disease progressed. Given earlier findings that the small molecule NAD⁺ plays an important role in aging, the team evaluated whether augmenting NAD⁺ could modulate REST levels.
In mouse models of Alzheimer’s disease, administering NAD⁺ increased REST activity in the brain, slowed memory loss, and improved waste clearance. Experimental elevation of REST within one side of the hippocampus was associated with lower amyloid‑beta deposition compared with the contralateral side, consistent with enhanced removal of toxic protein aggregates. The study's authors also note a broader hypothesis that age‑related inefficiency in autophagy, the brain’s waste‑removal system, contributes to neurodegeneration.
The study’s findings, published in Brain, position REST as both a mechanistic node and a candidate biomarker. Earlier research from King’s College London had suggested that REST could serve as a novel biomarker, and the present results further strengthen that association. The work was conducted at the Fang-Stavem Lab at the University of Oslo and Akershus University Hospital.
“We show for the first time that NAD⁺ can induce the activity of the protective protein REST in the brain. This strengthens the scientific basis for conducting NAD⁺ related clinical trials with patients,” said Associate Professor Evandro Fei Fang‑Stavem, University of Oslo.
“Our research further strengthens this link between lower REST levels and the development of Alzheimer’s disease”, said Beatriz Escobar-Doncel, a PhD student at the Fang-Stavem Lab at the University of Oslo and Akershus University Hospital.
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University of Oslo
Akershus University Hospital
