The buildup of amyloid beta plaques in Alzheimer’s disease is believed to result from patients’ inability to break down the protein. But a new study from Lund University, Sweden, showed that overproduction of amyloid beta is more common than previously thought, giving a more nuanced picture of Alzheimer’s pathology.
A small number of Alzheimer’s patients overproduce amyloid beta because of a genetic mutation, leading to the disease. In the majority of patients, however, the mechanisms behind the accumulation of amyloid beta in the brain are not clear, although the prevailing theory has been that of impaired protein breakdown.
“In our study, we show that accumulation of amyloid in the brain is associated with high levels of specific amyloid peptides in the cerebrospinal fluid. This means that overproduction of amyloid beta may contribute to development of Alzheimer’s disease in some people, even if they do not carry the hereditary risk gene for Alzheimer’s. The fact that the disease in these individuals can be attributed to both the overproduction of and problems in breaking down amyloid beta may be of significance to the future development of drugs and treatments,” Niklas Mattsson, one of the researchers behind the study, said in a press release.
The study, titled ”Increased amyloidogenic APP processing in APOEε4-negative individuals with cerebral β-amyloidosis” and published in Nature Communications, investigated amyloid beta in 331 people with mild cognitive disorders — a potential early sign of Alzheimer’s disease — and in healthy controls. The team used three complementary methods to measure the processing of amyloid beta: cerebrospinal fluid sample analysis, PET scanning, and genetic analysis.
“The results are important because they increase the understanding of how Alzheimer’s disease arises. Our hope is that this and other similar studies can increase the possibilities of personalising treatments that slow down the disease in the future,” said Oskar Hansson, a reader at Lund University and consultant at Skåne University Hospital.
Researchers said that while the study was limited by not including direct observations of participants’ brain tissue, the three complementary methods used to assess amyloid beta are likely to produce robust results. The study also included a relatively large group of participants, but the authors agree that more research is needed to verify the results.
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