Applicability Of Our Monoclonal Antibodies
Early-Stage Precision Diagnostics
Parkinson’s disease is a progressive neurological disorder that often remains undetected until significant and irreversible damage to dopamine-producing neurons has already occurred. Today, diagnosis typically relies on clinical symptoms such as tremors, rigidity, and impaired movement—signs that emerge only after the majority of these neurons have been lost. By this stage, therapeutic options are limited to symptom management rather than interventions that could alter disease progression. Early-stage precision diagnostics offer a transformative shift in how Parkinson’s disease is understood and treated. By using monoclonal antibodies developed by Core-Oli-T AB, subtle biological changes long before clinical symptoms can be visualized. This allows for earlier intervention, improved patient stratification in clinical trials, and more personalized treatment strategies. With accurate early detection, patients benefit from targeted therapies, lifestyle adjustments, and neuroprotective approaches while they still have the greatest potential impact. Investing in early, precise detection is essential to slowing disease progression, improving quality of life, and ultimately changing the trajectory of Parkinson’s disease.
Figure 1. Our antibodies can be used for early-stage precision diagnostics. A blood plasma sample from whole blood (1, top panel, left hand side) or cerebrospinal fluid (CSF) (2, bottom panel, left hand side) is taken from the patient. The sample is then transferred to a well plate together with our fibril-specific monoclonal antibodies (FS-mAbs) that are individually labeled with different color fluorophores (top panel, right hand side). The relative abundance of the different fibril structures found in the patient sample is then analyzed (bottom panel, right hand side). The outcome from this simultaneous measurement can help the doctor to more effectively treat the patient to minimize disease symtoms thereby increase the patient’s life quality.
Late-Stage Brain Imaging
Understanding neurological diseases requires precise visualization of biological processes inside the brain, yet current imaging tracers often lack the specificity needed to detect early molecular changes. Traditional small-molecule tracers can struggle to distinguish between closely related proteins or to target low-abundance pathological markers, limiting their utility in diseases such as Parkinson’s. As a result, the disease is often diagnosed late, when neuronal damage is already extensive and therapeutic options are less effective. Antibody-based tracers offer a powerful new approach. By leveraging the inherent specificity of monoclonal antibodies, these tracers can bind precisely to disease-relevant targets—such as misfolded proteins. When combined with advanced imaging modalities like PET , antibody tracers enable real-time visualization of disease processes at the molecular level. This improved precision supports earlier detection, better monitoring of disease progression, and more accurate evaluation of therapeutic responses. Advancing antibody-based imaging is key to moving brain research from symptom-focused diagnoses to truly mechanism-driven precision medicine.
Figure 2. Our antibodies can be used for late-stage brain imaging. To provide further tools for brain imaging, for patients demonstrating symtoms for late-stage Parkinson’s disease, our tracers-marked antibodies can help the medical doctor not only to draw conclusions regarding the patient’s brain status but also to specifically know what alpha-synuclein fibriltype that cause brain degeneration. A tracers-labelled fibril-specific monoclonal antibody is given to a patient prior to a PET-scan (1). Analysed data (2) can determine what fibril type that causes disease. Despite the need for individual assays, our monoclonal antibody portfolio can be used to detect the presence of multiple disease causing or non toxic fibril types.
Therapeutics – The Holy Graal
Parkinson’s disease is driven by complex molecular processes, including misfolding and aggregation of alpha-synuclein, neuroinflammation, and progressive degeneration of dopaminergic neurons. Current therapies primarily address symptoms by improving motor function or compensating for dopamine loss, but none directly target the underlying biological mechanisms responsible for disease progression. As a result, patients continue to experience worsening neurological function despite treatment. Antibody-based therapeutics offer a promising approach to modify disease progression at its source. Highly selective monoclonal antibodies can be engineered to bind pathological forms of alpha-synuclein, prevent their aggregation, and enhance clearance through immune-mediated pathways. They can also be designed to target inflammatory mediators or other molecular drivers of neurodegeneration, enabling precise modulation of disease biology. These targeted mechanisms open the door to disease-modifying therapies rather than symptomatic relief alone. In addition, antibody-based strategies can be paired with biomarkers and imaging tools to confirm target engagement, stratify patients based on disease biology, and support personalized therapeutic approaches. Investing in antibody-based treatments for Parkinson’s disease is critical to developing interventions that slow, halt, or potentially reverse neurodegeneration—shifting the therapeutic landscape from management to true modification of disease progression.
Figure 3. Monoclonal antibodies developed by our innovative strategy can potentially be used to treat Parkinson’s disease patients more efficiently. We are in the current process of developing fibril-specific monoclonal antibodies with applicability for diagnostic purposes but the longterm aim is to generate treatments that slow down disease progression or optimally completeley inhibit its development.
Scientific papers that lead to development of our antibodies
The following articles present research focused on a novel approach for developing antibodies targeting Parkinson’s disease.
Paper I
Amyloid Fibrils Prepared Using an Acetylated and Methyl Amidated Peptide Model of the Alpha-Synuclein NAC 71-82 Amino Acid Stretch Contain an Additional Cross-Beta Structure Also Found in Prion Proteins
Authors: Thomas Näsström, Per Ola Andersson, Christian Lejon,
and Björn C. G. Karlsson.
Journal: Scientific Reports
Volume/Starting page/Year: 9, 15949, 2019
Read at the publisher: https://doi.org/10.1038/s41598-019-52206-5
Paper II
A Capped Peptide of the Aggregation Prone NAC 71–82 Amino Acid Stretch of Alpha-Synuclein Folds into Soluble Beta-Sheet Oligomers at Low and Elevated Peptide Concentrations
Authors: Thomas Näsström, Jörgen Ådén, Fumina Shibata, Per Ola Andersson,
and Björn C. G. Karlsson.
Journal: International Journal of Molecular Sciences
Volume/Starting page/Year: 21, 1629, 2020.
Read at the publisher: https://doi.org/10.3390/ijms21051629
Paper III
Synthetic NAC 71-82 Peptides Designed to
Produce Fibrils with Different Protofilament Interface
Contacts
Authors: Thomas Näsström, Tobias Dahlberg, Dmitri Malyshev, Jörgen Ådén,
Per Ola Andersson, Magnus Andersson, and Björn C. G. Karlsson.
Journal: International Journal of Molecular Sciences
Volume/Starting page/Year: 22, 9334, 2021.
Read at the publisher: https://doi.org/10.3390/ijms22179334
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