A new study has identified higher levels of the protein meprin-β in the brains and cerebrospinal fluid of people with Alzheimer's disease, adding to growing evidence that the enzyme may be linked to biological processes underlying the condition. The findings, published in Alzheimer's Research & Therapy, suggest that the active form of meprin-β becomes increasingly elevated as Alzheimer's disease progresses. Researchers say the results point to a possible connection between the protein and the buildup of beta-amyloid, one of the defining features of Alzheimer's.
The condition currently has no known cure, but researchers hope the findings can offer a new indicator of the disease that could be used to test for treatments in the future. "This study adds an important piece to our understanding of the complex biology behind Alzheimer's disease," Dr. Steven Chance, founder and chief scientific officer at Oxford Brain Diagnostics, told Newsweek.
"Fluid biomarkers can help identify signs of Alzheimer's, such as amyloid buildup, but they don't tell us how early the brain is affected or how its structural integrity changes over time. "The finding that active meprin-β increases primarily in the more advanced stages of disease raises an important next question: how do molecular changes like these relate to what is actually happening in the brain as Alzheimer's progresses?" He added that combining biomarker research with quantitative brain imaging could help researchers link biological changes to measurable alterations in brain structure throughout the course of the disease. Alzheimer's disease is characterized by the accumulation of beta-amyloid plaques in the brain.
These plaques form when amyloid precursor protein (APP) is broken down by enzymes. One of the best-known enzymes involved in this process is beta-secretase 1 (BACE1), but researchers have investigated other enzymes that can act as beta-secretases, including meprin-β. To better understand the protein's role, scientists analyzed meprin-β in brain tissue samples taken from people at different stages of Alzheimer's disease.
The team examined the protein's immature, inactive form separately from its mature, active form. The samples came from the frontal cortex and were classified according to Braak stages, a system used to measure the progression of Alzheimer's-related pathology in the brain. Researchers found that levels of the active form of meprin-β increased in patients with more advanced disease.
This pattern was not seen in the earliest stages of Alzheimer's. They also detected elevated levels of MEP1B messenger RNA, the genetic template that instructs cells to produce the protein, during intermediate and advanced stages of the disease. The researchers then examined cerebrospinal fluid samples and found increased levels of active meprin-β in people with Alzheimer's disease.
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