A blood test can now estimate when ALS symptoms will begin in people who carry an ALS-linked gene, landing on average within about 18 months of the real onset date, according to a study published July 27, 2026 in Nature Medicine. NIH-funded researchers at the University of Miami measured more than 5,000 proteins in blood samples collected over years of follow-up, then narrowed the list to a 19-protein panel that tracks the switch from healthy carrier to patient.
Key takeaways
- A 19-protein blood panel estimated the time until ALS or frontotemporal dementia symptoms started, with an average error of 1.6 years.
- The panel was built in 137 people from the Pre-fALS study, a cohort of gene variant carriers followed for nearly 20 years.
- It was developed almost entirely in people with a known ALS gene, so it is not yet a screening test for the general public.
What the study found
The team analyzed 516 blood samples from 137 participants: 33 people who went on to develop clinically apparent ALS or frontotemporal dementia, 35 people who already had ALS, 10 carriers who had not yet converted, and 59 controls, according to the study in Nature Medicine.
Having measured levels of more than 5,000 proteins, the researchers found 92 whose levels changed before any symptoms appeared. Machine learning trimmed that to a core set of 19.
That panel predicted conversion across time windows from 6 months to 5 years out. Its accuracy score ran from 0.80 to 0.89 (cross-validated area under the curve), which means that if you compared one person who was about to convert with one who was not, the panel ranked the right person as higher risk roughly 80 to 89 percent of the time. Its estimate of when symptoms would start was off by 1.6 years on average, which is where the 18-month figure in the NIH release comes from.
The findings were partly replicated in UK Biobank data, which confirmed presymptomatic rises in several proteins including NEFL, EDA2R and CA3, and confirmed that the multi-protein panel beat NEFL (neurofilament light) on its own. The work was funded by NINDS grants R01NS105479 and U54NS092091.
Dr. Kumar’s take
Handing a healthy person a date for a disease with no cure is a heavy thing to do, and I would not want that framing to be the headline. In clinic, a number like this cuts both ways. Some people want the date so they can plan work, finances and family. Others are living reasonably well with uncertainty, and a prediction with an 18-month error bar can steal that without giving anything back.
The real value here is not counseling. It is trial design.
Presymptomatic drugs only work if you can find people who are about to convert. Tofersen, approved for symptomatic ALS, is being tested as a preventive therapy in the ATLAS trial, which was designed by the same investigator who led this work, per the NIH release. Until now that kind of trial has leaned heavily on neurofilament light, which rises fairly late and mostly in fast-progressing SOD1 carriers. A panel that outperforms NEFL and works across a wider set of variants means smaller, faster, cheaper prevention trials. That is the bottleneck this addresses, and it is a real one.
The caveat most coverage will skip: this was built in people already known to carry a pathogenic variant. Roughly 90 percent of ALS is sporadic, with no family history and no gene to test. Nothing here tells a person without that genetic context anything yet. The converter group was also small at 33 people, and the UK Biobank replication was partial, not complete. This is a research tool that needs prospective validation, not a test to ask your doctor for.
What it means for you
If you carry an ALS-associated gene and are followed in a research program, ask your neurologist whether trials like ATLAS are recruiting, and whether biomarker sampling is part of your visits. That is how these panels get validated and how you get access early.
If you do not have a family history of ALS, this changes nothing about your care today. It is a good example of a broader shift though: blood proteins and cell-free DNA are increasingly picking up disease before symptoms, the same way a new blood test detects liver disease before symptoms appear, and the same reason researchers now track protective proteins in the blood as a marker of diet quality.
ALS now has a measurable window before symptoms start. Turning that window into a treatment is the next job.