Khaberni - Despite decades of research focused on eradicating beta-amyloid protein clumps in the brains of those with Alzheimer's disease, considering it the key to treatment, a recent study reveals that this approach may not be sufficient to address the core issue.
According to new research conducted by scientists from Osaka Metropolitan University in Japan, removing these plaques does not rejuvenate the brain's system responsible for waste disposal, known as the glymphatic system, which relies on cerebrospinal fluid waves to wash excess proteins from the brain.
It is known that this system is clearly malfunctioning in Alzheimer's patients.
The study, which involved 13 patients treated with the new anti-amyloid drug Lecanemab, used magnetic resonance imaging scans to monitor changes within the brain.
Researcher Tatsushi Ora said, "Even with reduced beta-amyloid levels due to treatment, the glymphatic system does not appear to recover quickly."
The results highlight the complex and multifaceted nature of Alzheimer's; as scientists are still unable to determine whether amyloid plaques and tau protein are a direct cause of the disease or one of its outcomes, according to "Science Alert".
Although Lecanemab was successful in reducing amyloid accumulation, the study clarified that indicators of glymphatic system function did not improve after three months of treatment.
The research team wrote: "Disease-modifying treatments may reduce plaques and slow cognitive decline, but they do not reverse existing neurological damage."
These findings are not the first to lead some researchers to believe that plaques may be a symptom of the disease, not its primary cause.
Previous trials indicate that the effectiveness of Lecanemab is most apparent at the very early stages of Alzheimer’s; pushing for more attention to the early detection of dementia indicators.
