A study has found increased levels of the active protein meprin-β in the brains and cerebrospinal fluid of individuals with Alzheimer's disease.
Key facts
- •The study was led by Javier Sáez Valero of the Institute for Neurosciences, a joint center of Miguel Hernández University of Elche and the Spanish National Research Council.
- •Meprin-β acts as a β-secretase, an enzyme involved in processing amyloid precursor protein (APP) into beta-amyloid.
- •Researchers observed that active meprin-β levels rise in the brain and cerebrospinal fluid as Alzheimer's disease progresses to advanced Braak stages.
- •Experiments showed that exposing human neurons to the beta-amyloid peptide Aβ42 triggers an increase in meprin-β levels.
- •The research team included collaborators from the University Medical Center Mainz, the University of Barcelona, and the University of Gothenburg.
A research team led by Javier Sáez Valero at the Institute for Neurosciences in Spain has discovered that the active form of the protein meprin-β is elevated in patients with Alzheimer's disease. The findings, published in Alzheimer's Research & Therapy, suggest a potential link between this enzyme and the accumulation of beta-amyloid, a hallmark of the condition. The study involved analyzing brain tissue and cerebrospinal fluid samples to track how the protein changes throughout the disease's progression.
Protein Levels and Disease Progression
Researchers examined frontal cortex samples from individuals at various stages of Alzheimer's, classified by Braak stages. They found that the active form of meprin-β increases specifically during the more advanced stages of the disease, whereas no such increase was observed in early stages. Additionally, the team detected higher levels of MEP1B messenger RNA—which provides the instructions for producing the protein—in both intermediate and advanced stages of the pathology.
Cerebrospinal Fluid and Experimental Links
The study also identified increased levels of active meprin-β in the cerebrospinal fluid of patients, a finding the researchers note could be significant because this fluid can be accessed via lumbar puncture to monitor nervous system changes. To further investigate the relationship between the protein and beta-amyloid, the team tested transgenic rats and human neurons derived from induced pluripotent stem cells. When human neurons were exposed to the beta-amyloid peptide Aβ42, the researchers observed a significant increase in meprin-β, providing an experimental connection between the two.
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This article was independently rewritten by ManyPress editorial AI from reporting originally published by Medical Xpress.
