Scientists may have found the true cause of Alzheimer’s disease — and believe the condition can be detected using a simple blood test.
Experts have long known the build-up of amyloid in the brain is linked to the disease, but whether the plaques are a cause or a symptom has remained a mystery.
Even more puzzling is why some patients with amyloid clumps in their brains never go on to develop Alzheimer’s. Now a ‘game-changing’ study by the University of Pittsburgh claims to have the answer.
They found patients who go on to develop Alzheimer’s also have indicators in their blood that immune cells called astrocytes are activated.
These star-shaped immune cells supply the brain with nutrients and oxygen and protect it from pathogens.
Dr Tharick Pascoal, associate professor of psychiatry and neurology at the university and the study’s senior author, said: ‘This puts astrocytes at the center as key regulators of disease progression, challenging the notion that amyloid is enough to trigger Alzheimer’s disease.
The study was published in the journal Nature Medicine.
The team tested the blood of more than 1,000 cognitively healthy older adults with and without amyloids in their brain.
They found that only those who had a combination of amyloid and blood markers of abnormal astrocyte activity would progress to symptomatic Alzheimer’s in the future.
They described it as a ‘critical’ discovery for drug development aimed at halting progression.
Professor Pascoal said: ‘Our study argues that testing for the presence of brain amyloid along with blood biomarkers of astrocyte reactivity is the optimal screening to identify patients who are most at risk for progressing to Alzheimer’s disease.
The hallmark of Alzheimer’s is an accumulation of amyloid plaques – protein aggregates lodged between nerve cells of the brain – and clumps of disordered protein fibers, called tau tangles, forming inside the neurons.
For many years brain scientists believed that an accumulation of amyloid plaques and tau tangles is not only a sign of Alzheimer’s disease but also its direct culprit.
The assumption also led drug manufacturers to invest heavily in molecules targeting amyloid and tau, overlooking the contribution of other brain processes, such as the neuroimmune system.
These star-shaped immune cells supply the brain with nutrients and oxygen and protect it from pathogens.
Dr Tharick Pascoal, associate professor of psychiatry and neurology at the university and the study’s senior author, said: ‘This puts astrocytes at the center as key regulators of disease progression, challenging the notion that amyloid is enough to trigger Alzheimer’s disease.
The study was published in the journal Nature Medicine.
The team tested the blood of more than 1,000 cognitively healthy older adults with and without amyloids in their brain.
They found that only those who had a combination of amyloid and blood markers of abnormal astrocyte activity would progress to symptomatic Alzheimer’s in the future.
They described it as a ‘critical’ discovery for drug development aimed at halting progression.
Professor Pascoal said: ‘Our study argues that testing for the presence of brain amyloid along with blood biomarkers of astrocyte reactivity is the optimal screening to identify patients who are most at risk for progressing to Alzheimer’s disease.
The hallmark of Alzheimer’s is an accumulation of amyloid plaques – protein aggregates lodged between nerve cells of the brain – and clumps of disordered protein fibers, called tau tangles, forming inside the neurons.
For many years brain scientists believed that an accumulation of amyloid plaques and tau tangles is not only a sign of Alzheimer’s disease but also its direct culprit.
The assumption also led drug manufacturers to invest heavily in molecules targeting amyloid and tau, overlooking the contribution of other brain processes, such as the neuroimmune system.