The science behind NeuroQuestOur technology is where intellectual property, laboratory and clinical research come together
Our technology uses immune cells from peripheral blood as biomarkers to screen for pre-clinical signs of Alzheimer’s. NeuroQuest licensed the intellectual property covering this technology from Yeda (the Weizmann Institute Technology Transfer Arm), and holds exclusive global rights for its development and commercialization.
NeuroQuest has developed a unique blood-based diagnostic test for Alzheimer’s based on the specific response of the immune system. The test is based on the highly acclaimed research work of Prof. Michal Schwartz, Chair of Neuroimmunology at the Weizmann Institute, whose research group has pioneered work in the field of neuroimmunology for more than a decade.
Clinical trial data
A recent exploratory study with the Australian Imaging, Biomarker, and Lifestyle Flagship Study of Aging demonstrated the ASSAY has more than 90 percent sensitivity and 80 percent specificity in diagnosis of beta-amyloid positive. This surpasses the minimum 80 percent sensitivity and specificity criteria for ideal biomarkers as defined by the U.S. Alzheimer’s Association.
How our technology becomes a surrogate for PET scans
Immunosuppressive cell populations as biomarkers
Alzheimer’s is currently defined as: Dementia with beta-amyloid plaques in the brain. Based on that definition, PET imaging for beta-amyloid plaques – as shown on the right – represents the standard for confirmatory diagnosis of beta-amyloid.
Our science shows immunosuppressive cell populations in Alzheimer’s are key players in the inability of the body to mount a systemic immune response needed for mitigation of disease pathology. Our blood-based biomarker test measures peripheral changes in myeloid cell populations resulting in a highly translatable, relatively high-throughput and cost-effective diagnostic surrogate for PET-amyloid status diagnosis.
The deep dive into immunosuppressive cell populations
The choroid plexus - a key factor in brain inflammation
Professor Schwartz’s research group suggested that recruitment of inflammation-resolving immune cells to the diseased brain is needed for arresting neuroinflammation, and is dependent on the activity of the choroid plexus (CP), which may dysfunction under brain pathologies. Their research showed that in brain aging the CP displays an IFN type I (IFN-I) response signature, including a dramatic rise of IFN-β expression. They also showed that by rejuvenating the blood composition of aged mice, CP activity is amendable for restoration and the effect was associated to partial restoration of cognitive function.
Current research shows, CP gateway activity for allowing immune cells to traffic the CNS is suppressed along disease progression. The findings show that circulating immune cell populations, with immunosuppressive functions, dramatically affect CP function. Specifically, systemic Foxp3+CD4+ Treg-mediated immunosuppression as a negative player in AD pathology, acting at least in part by interfering with IFN-γ-dependent activation of the CP, which is needed for orchestrating recruitment of inflammation-resolving leukocytes to the CNS.
Using genetic conditional ablation of Foxp3+ Treg cells in AD-Tg mice, and various pharmacological approaches to target these cells, Schwartz’ findings show that activation of the CP for supporting leukocyte trafficking to the CNS is followed by accumulation of immunoregulatory cells at cerebral sites of Aβ pathology, plaque clearance, and mitigation of cognitive decline.