Changes in levels of a protein in the blood could help shed light on damage in the brain more than a decade before symptoms of Alzheimer’s disease develop, researchers have revealed.

While there is no drug to stop the progression of Alzheimer’s, or cure it, the researchers said the study findings could be used by doctors to help anticipate when patients might start to show symptoms of the disease.

They also said it showed that measuring changes in levels of this protein in the blood was a useful way to test whether new Alzheimer’s drugs show promise – something researchers have already begun to embrace.

“We know Alzheimer’s disease starts [in the brain] one or two decades before you have any symptoms,” said Prof Mathias Jucker, a co-author of the study from the German Center for Neurodegenerative Diseases in Tübingen. “We also know any therapy has to interfere 10 years [before symptoms] or even earlier to be successful if you want to target the cause of Alzheimer’s disease.” The blood test, he said, would allow researchers to test whether drugs were having an effect.

Writing in the journal Nature Medicine, the team described how they looked at levels of a protein called neurofilament light chain (NfL) in participants’ blood and spinal fluid. This protein occurs inside neurons: previous research has shown increased levels of NfL in such fluids of mice to be linked to greater levels of damage to the brain, while Jucker added studies in humans had previously suggested NfL could be a useful marker for the progression of Alzheimer’s disease and other neurological conditions.

In total the team looked at NfL levels for 243 people carrying a genetic mutation that predisposed them to Alzheimer’s, and 162 people without such a mutation. Jucker noted people with these mutations developed symptoms of Alzheimer’s at well-defined ages, allowing the team to measure levels of NfL a known number of years before symptoms were expected to become apparent.

The team found about 6.8 years before symptoms developed, levels of NfL in the fluids began to markedly differ, with higher levels seen among those with a mutation of interest than those without, both in the blood and spinal fluid.

The team then looked at data from a smaller group of participants to see how levels of this protein in the blood changed over a period of about three years.

The results show the rate of increase in levels of NfL was higher for people genetically predisposed to Alzheimer’s than those without a mutation of interest, with differences apparent more than 16 years before symptoms were expected to be seen. What is more, the rise in NfL was steepest in the years prior to the onset of symptoms, before levelling off as symptoms emerged.

“It is not necessarily the absolute levels which tell you your neurodegeneration is ongoing, it is the rate of change,” said Jucker. “This rate of change [is] really sensitive very, very early – and that is exactly what we need for clinical studies.”

Further work suggests a higher level of NfL in the blood, and a steeper rise in NfL, might both be linked to faster levels of thinning of a region of the brains’ cortex known to be affected by Alzheimer’s, as well as faster decline in memory and cognition.

However, Dr James Pickett, the head of research at the Alzheimer’s Society, noted the study had limitations, including that it only looked at those who had a genetic predisposition to Alzheimer’s – which only affects 1% of those with the condition. Many other conditions can also increase levels of NfL, including traumatic brain injury and multiple sclerosis, meaning it is not clear how useful the measure would be among individuals living with multiple health problems.

Even so, Pickett, said the research was helpful. “We have done much to improve diagnosis rates but still only two-thirds of the 850,000 people across the UK living with dementia have a diagnosis, so any progress we can make to more accurately and quickly detect who has the condition is very welcome.”