Alzheimer’s is frequently diagnosed too late, but a new test can detect amyloid beta aggregation early on. While there is currently no cure an early diagnosis can help delay disease progression
Although researchers still aren’t entirely sure what causes Alzheimer’s, or if there even is a singular cause, in the majority of cases a peptide called amyloid beta clumps together. This forms the obvious amyloid plaques characteristic of the disease. Researchers hope that if we can gain a better of understanding of how this aggregation occurs, it might lead to better diagnosis and treatment.
New research from a collaborative team has found that in the early stages of aggregation, amyloid beta can actually fragment at specific points without any help from enzymes. These fragments are truncated, which means they’re shortened, and appear to bind to normal amyloid beta – inducing toxic oligomer formation. Abnormal cleavage also occurs when cellular enzymes process amyloid beta incorrectly, leaving similar reactive peptides that increase aggregation.
Screening mice with an Alzheimer’s model and post-mortem brain tissue, the team found this independent fragmentation of amyloid beta occurs in a particular pattern, producing a signature that can be detected. This form of enzyme independent fragmentation is a new discovery, but could also be used to both detect, and even fight Alzheimer’s progression by developing antibodies to these predictable fragments; allowing immune clearance.
“The study reveals novel Abeta targets associated with the early events of oligomerization. This may help define the preclinical stage of Alzheimer’s, and determine the factors that predict the emergence of clinical impairment and progression to severe dementia”
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