
Unlocking Neurological Disease with Comprehensive,
High-Sensitivity Protein Detection
With comprehensive profiling of Tau proteins—including both brain-specific and peripheral pTau217, pTau181, pTau231 and MAPT, —NULISA provides powerful insights into the disease heterogeneity of tauopathies. Beyond tau coverage, NULISAseq CNS Disease Panel 120 includes multiplex detection of important biomarkers across amyloid pathology, neurodegeneration, inflammation, synaptic and vascular processes.
By leveraging multiplexed assays for proteins implicated in neurodegenerative and inflammatory pathways, researchers and clinicians can now gain unprecedented insight into the molecular fingerprints that define distinct neurological disorders. This approach not only supports early diagnosis but also enables nuanced monitoring of disease progression, response to therapies, and patient stratification—paving the way for truly personalized interventions.
Alzheimer’s Disease and Dementia Research
Given the heterogeneous pathology of AD and mixed dementia, inflammation, synaptic, and vascular markers can play a key role in understanding disease pathophysiology. By measuring multiple CNS proteins simultaneously, Alamar’s ultra-sensitive NULISA™ multiplex panels can monitor changes across key processes to provide insights beyond the established AT(N) biomarkers. Karikari, et al. demonstrates how multiplexed, blood-based profiling can provide a comprehensive view of AD-associated proteomic changes, consistent with the recently revised biological and diagnostic framework.
What the data shows:

In addition to p-tau217 fourteen markers were shown to be significantly decreased in Aβ-PET + participant including TIMP3, BDNF, MDH1, and several cytokines. Longitudinally, FGF2, IL4, and IL9 exhibited Aβ PET-dependent yearly increases in Aβ-PET + participants.
Novel plasma biomarkers associated with longitudinal changes in tau PET identified proteins associated with neuroinflammation, synaptic function, and cerebrovascular integrity including; CHIT1, CHI3L1, NPTX1, PGF, PDGFRB, and VEGFA.
Frontotemporal Dementia (FTD)
The identification of reliable blood-based biomarkers that can distinguish frontotemporal dementia (FTD) from other neurodegenerative conditions is crucial. Recent research has demonstrated the efficacy of ultra-sensitive NULISA™ multiplex panels in detecting proteomic signatures in serum and plasma. These include key early disease biomarkers such as TDP-43, pTDP-43, NfL, Tau, and others associated with FTD pathology.
What the data shows:
Ashton, et al. identified of over 60 differentially expressed plasma proteins. NfL exhibited the most significant fold change, alongside Neurogranin, superoxide dismutase, and TDP-43, underscoring their potential as translatable biomarkers in sporadic FTD.
Malpetti, et al. observed lower levels of CRH and NfL in FTD patients; elevated levels of PSEN1, PARK7, and PGK1—associated with amyloid processing and metabolic dysregulation as well as a strong correlation between plasma NfL and survival in FTD and PSP, validating its utility for disease monitoring and trial endpoints. Several inflammation biomarkers from the NULISA inflammation panel were also elevated in FTD patients, with AREG and CD276 showing the most significant increases. Additional upregulated biomarkers included TREM2, Lamp3, CCL7, IL-17A and IL-17F.
Lewy Body Dementia / Dementia with Lewy Bodies (LBD/DLB)
The development of blood-based biomarkers to distinguish DLB from Alzheimer’s disease (AD) and other neurodegenerative disorders remain an urgent need. Recent publications have shown the utility of the ultra-sensitive NULISA multiplex panels simultaneously profile both known and novel biomarkers to discover blood-based proteomic signatures associated with DLB that distinguish between AD and DLB.
What the data shows:
Ashton, et al. carried out NULISAseq analysis in plasma samples of LB SAA+ versus AD SAA– patients showing 15 differentially changed proteins between symptomatic patients with and without αSyn pathology. After multiple testing correction, Aβ42 & VEGF vascular endothelial growth were seen to be upregulated with both p-tau217, & ENO2 being downregulated.
Malpetti, et al. used NULISA CNS Disease & Inflammation Panels to simultaneously profile NfL, GFAP, p-tau217, p-tau231, and p-tau181 in LBD and AD patients. Beyond the common dementia-relevant markers – CRH emerged as a biomarker of interest with lower levels strongly associated with worse survival in LBD patients.
Progressive Supranuclear Palsy (PSP)
The development of blood-based biomarkers to distinguish PSP from other neurodegenerative disorders is an urgent need. In a recent publication, Malpetti, et al. showcased the utility of ultra-sensitive NULISA multiplex panels for simultaneous profiling across key CNS Disease & Inflammation biomarkers to identify disease-specific patterns in serum samples.
What the data shows:
Serum NfL levels are promising blood-based biomarkers for tracking disease progression and prognosis in PSP, outperforming other markers like p-tau217, p-tau231, and GFAP. PSP patients show increased proinflammatory proteins (OSM, MMP9, CCL7) and anti-inflammatory proteins (CD276, AREG), with IL1RN and HGF also elevated. Additional markers such as SQSTM1 and PSEN1 are higher in PSP and help distinguish it from AD/MCI+. New assays targeting brain-derived tau proteins (MAPT, pTau217, pTau181, pTau231) expand the capabilities of the NULISAseq CNS Disease 120 Panel for identifying blood-based biomarkers in PSP.