What's Happening?
A new study shows that clearing away the amyloid-beta clumps doesn't appear to repair key brain functions in Alzheimer's patients. The study, conducted by researchers at Osaka Metropolitan University in Japan, tested the new Alzheimer's drug lecanemab
on 13 people with the disease. While lecanemab reduced amyloid-beta levels in the brain, measures of glymphatic system function did not improve after three months.
Why It's Important?
The study highlights the multifaceted nature of Alzheimer's, which is associated with a wide range of potential causes, risk factors, and symptoms. It suggests that while disease-modifying therapy can reduce plaque burden and slow further cognitive worsening, it does not restore lost function. This reflects the fact that neuronal damage and clearance system deficits have already been well established.
What's Next?
Researchers are keen to expand the study parameters, looking at how lecanemab affects Alzheimer's at different stages or when administered for longer. Future research will focus on understanding the best way to administer treatment to patients, considering factors like age, the stage of the disease, and degree of lesions in the white matter.
Beyond the Headlines
The study adds more nuance to the increasingly complex picture of Alzheimer's, and how it might be tackled. Some researchers are now suspecting the plaques are a consequence of the disease, not the cause. Past trials have shown that lecanemab works best when administered at an early stage, emphasizing the importance of early detection.
