Alzheimer’s Disease Could Be Detected 11 Years Early With New Blood Biomarker
Beta-synuclein levels in blood rise up to 11 years before Alzheimer’s symptoms, offering an early diagnostic tool.
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Recent research published in Alzheimer’s & Dementia reveals that individuals with a genetic predisposition to Alzheimer's disease exhibit altered blood levels of beta-synuclein, a protein linked to neuronal damage, as early as 11 years before dementia symptoms typically emerge. The study, involving a team of researchers from DZNE, Ulm University Hospital, and University Medicine Halle, highlights the potential of beta-synuclein as an early biomarker for neurodegeneration. Early identification of such biomarkers could be crucial for initiating treatment when it is most effective.
Beta-synuclein
Beta-synuclein is a protein found in the brain, particularly in synapses, where it plays a role in regulating neurotransmitter release. In Alzheimer’s disease, synaptic degradation causes beta-synuclein to be released into the bloodstream, making it a potential marker for early neurodegeneration.
Neurodegeneration
Neurodegeneration refers to the progressive degeneration of the structure and function of the nervous system. Alzheimer’s disease is a major cause of neurodegeneration, leading to memory loss, cognitive decline and eventually dementia.
The need for early diagnosis in Alzheimer’s disease
Alzheimer’s disease, the leading cause of dementia, is often diagnosed late in its progression, typically when cognitive decline is already evident. The recent approval of amyloid antibody drugs – designed to remove harmful brain deposits – has underscored the importance of early-stage treatment. However, these treatments require early diagnosis to be effective. Dr. Patrick Öckl, a leader in the research group, emphasized that the late diagnosis of Alzheimer’s means that the full potential of these new drugs is not yet being realized. He and his colleagues have been investigating beta-synuclein because its presence in blood reflects neuronal damage, and its levels can be easily measured. This study provides further support for the potential of beta-synuclein as an early diagnostic tool. In addition to Alzheimer’s, this protein could also indicate neuronal damage resulting from other conditions, such as stroke.
The role of beta-synuclein in synaptic degeneration
Beta-synuclein is primarily found in synapses, the connections between neurons where signals are exchanged. In Alzheimer’s disease, synapses begin to deteriorate, releasing beta-synuclein into the bloodstream. The researchers found that this synaptic breakdown starts long before cognitive impairment becomes apparent, making beta-synuclein a valuable marker of pre-symptomatic neurodegeneration. As beta-synuclein levels rise, they signal that synaptic damage is occurring, potentially years before the onset of symptoms.
Synapse
A synapse is the junction between two neurons, where chemical signals are transmitted to allow communication between them. In Alzheimer’s disease, synaptic loss and dysfunction contribute to cognitive decline.Study of familial Alzheimer’s disease and blood biomarkers
This study focused on participants from the Dominantly Inherited Alzheimer’s Network (DIAN), which tracks genetic mutations linked to early-onset familial Alzheimer’s disease. This hereditary form of Alzheimer’s is rare but follows a clear genetic pattern, with symptoms often appearing in middle adulthood. Researchers could estimate the expected onset of dementia based on family history. The study tracked over 100 adults, aged in their 30s and 40s, with mutations that are almost certain to lead to Alzheimer’s. The blood levels of beta-synuclein were analyzed alongside cognitive performance tests, cerebrospinal fluid samples and brain scans.
The results showed that beta-synuclein levels began to rise about 11 years before the expected onset of symptoms in these individuals. This early biomarker corresponds with synaptic degeneration, which later manifests as cognitive impairment. As cognitive function declined, the beta-synuclein levels in the blood increased, reflecting the progression of the disease from the pre-symptomatic to the symptomatic stage.
The potential for broader applications
Although the study focused on the hereditary form of Alzheimer’s disease, Dr. Öckl speculated that similar patterns could be observed in the more common, sporadic form of the disease. If further studies confirm these findings, beta-synuclein could become an important tool for diagnosing Alzheimer’s earlier, potentially improving the effectiveness of new treatments. Moreover, it could be used to monitor the effects of therapies, assessing whether treatments are slowing down synaptic loss and disease progression.
The research demonstrates that beta-synuclein levels in blood could provide an early signal of Alzheimer’s disease, helping to identify individuals at risk long before clinical symptoms appear. This marker not only has diagnostic potential but could also serve as a tool to monitor the efficacy of therapies aimed at slowing neurodegeneration. Future studies are needed to verify these findings in a broader population, but beta-synuclein holds promise as a key biomarker in the fight against Alzheimer’s disease.
Reference: Oeckl P, Mayer B, Bateman RJ, et al. Early increase of the synaptic blood marker β‐synuclein in asymptomatic autosomal dominant Alzheimer’s disease. Alzheimer’s Dementia. 2025;21(4):e70146. doi: 10.1002/alz.70146
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