According to the Centers for Disease Control and Prevention (CDC), Alzheimer’s disease affects around 5.8 million Americans. The most prevalent kind of dementia is progressive dementia, which is characterized by memory loss and cognitive impairment in brain areas involved in reasoning, memory, and language.
Presently, there is no cure for Alzheimer’s, but emerging treatments like Leqembi, also known as Lecanemab, show promise in providing relief and slowing disease progression. The body’s immune system is also recognized as a potential ally in this battle.
The US Food and Drug Administration has granted full approval to the first Alzheimer’s drug that demonstrates the ability to slow the disease. Leqembi, an antibody treatment administered directly into the brain, effectively reduces amyloid beta—a protein forming plaques leading to brain cell death and shrinkage. Clinical trials have revealed a 27% slowdown in cognitive decline over 18 months.
However, a recent study by Dutch scientists introduces a twist to this narrative. They’ve identified five biological variants of Alzheimer’s, suggesting the need for different treatments. This new study challenges the efficacy of previously tested drugs, potentially rendering them ineffective or only minimally effective.
Researcher Betty Tijms and her team from Alzheimer Center Amsterdam, Amsterdam UMC, and Maastricht University presented these findings in the journal Nature Aging.
In Alzheimer’s disease, the brain experiences the aggregation of amyloid and tau proteins. Alongside these protein clumps, additional biological processes such as inflammation and nerve cell growth play a role.
Using innovative techniques, researchers have successfully measured these supplementary processes in the cerebrospinal fluid of individuals exhibiting amyloid and tau protein clumps.
In the study, 1058 proteins in the cerebrospinal fluid of 419 Alzheimer’s patients were scrutinized. The investigation revealed the existence of five distinct biological variants within this cohort.
The initial variant is distinguished by heightened amyloid production. The second variant is characterized by a disrupted blood-brain barrier, reduced amyloid production, and diminished nerve cell growth.
Additionally, these variants differ in protein synthesis levels, immune system functionality, and the performance of the organ responsible for cerebrospinal fluid production.
Patients with different Alzheimer’s variants exhibited variations in disease progression, with certain subgroups experiencing an accelerated course.
The results have significant implications for medication research. They indicate that a specific drug may only be effective in addressing one variant of Alzheimer’s disease.
For instance, a medication inhibiting amyloid production might be beneficial in the variant with increased amyloid production but could pose risks in the variant with decreased amyloid production.
Moreover, patients with one variant may have a higher risk of side effects, while those risks are considerably lower in other variants.
The study team’s next objective is to demonstrate that Alzheimer’s variations do respond differently to medications so that everyone will get the right care in the future.
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