Alicia Algeciras-Schimnich, Ph.D.

The purpose of this study is to evaluate the performance of various AD blood-based biomarkers including two pTau217 assays and an AB42/40 assay against the currently clinically available CSF AD biomarker assay (pTau181/AB42) for their ability to detect amyloid pathology in patients presenting with cognitive impairment.

The overall aim of this study is to evaluate the performance of blood-based biomarkers of Alzheimer's Disease (AD) in patients undergoing Lecanemab treatment at Mayo Clinic Rochester.  

Specific Aims:

• Evaluate the use of the plasma AD biomarkers: plasma amyloid beta 42/40 ratio (Abeta42/40) and phosphorylated Tau (pTau) to detect amyloid pathology in patients enrolled in Lecanemab infusion treatment (baseline measurement). In this aim the performance of these biomarkers to identify patients with a positive amyloid-PET or positive CSF biomarkers will be assessed.
• Evaluate changes in plasma AD biomarkers: plasma Abeta42/40 and pTau in patients enrolled in Lecanemab infusion treatment.  In this aim the blood biomarker concentrations will be evaluated longitudinally (baseline and then 3, 6, 12, 18 and 24 months after treatment initiation). The goal is to assess if changes in blood-based biomarkers correlate with treatment associated changes in clinical measures such as cognitive test scores, MRI and PET imaging and AD CSF biomarker measurements associated with amyloid pathology.
• Evaluate if changes in plasma biomarkers such as neurofilament light chain (NfL) and glial fibrillary acidic protein (GFAP) may be predictors of amyloid-related imaging abnormalities (ARIA) in patients enrolled in Lecanemab infusion treatments.  In this aim, these blood biomarker concentrations will be evaluated longitudinal (baseline and then 3, 6, 12, 18 and 24 months after treatment initiation) to assess if changes in blood-based biomarkers correlate with development of ARIA or other complications.  Additionally, these markers are associated with changes in amyloid pathology and will also be examined for correlation with Abeta42/40 and pTau blood-based biomarkers over the course of the study.

The purpose of this research is to evaluate a clinical assay designed to measure biomarkers that will help us understand COVID-19.

The purpose of this study is to validate the Alzheimer Disease Biomarkers assays (Phospho-Tau/Total-Tau/Ab42) being implemented at Mayo to compare them to the referral tests in support of test validation efforts.

The purpose of this study is to establish the clinical performance of the Medfrontier Intact FGF23 immunoassay in patients with tumor induced osteomalacia (TIO) and X-linked hypophosphatemia (XLH).

The purpose of this study is to correlate the parathyroid hormone-related peptide (PTHrp) levels in the current and new assays in patients with known disease and calcium status. 

Aim 1: Determine the basal profile of non-genomic factors in patients at the time of exposure to SARS-CoV-2 and correlate with the three clinical patient outcome categories (A, B, C) as observed through their clinical course. 

Hypothesis: Baseline cytokine (IL-1β, IL-6, IL-4, IL-10, IFN-g and TNF-a) and the immune cellular repertoire (helper/CD4+, cytotoxic/CD8+, T-regulatory cells, natural killer cells) constitute the inherent biologic immunity of an individual and underpins their vulnerability to SARS-CoV-2 infectivity and/or its subsequent sequalae. 

Aim 2: Investigate if mutations or polymorphisms in genes (CXCR6, ACE2 and SLC6A20) linked to SARS-CoV-2 correlates with the three clinical patient outcome categories (A, B, C) as observed through their clinical course.

Hypothesis: ACE2 is a cellular receptor for SARS-CoV-2. The high binding affinity of ACE2 to SARS-CoV-2 is determined by its gene sequence and polymorphisms in the ACE2 gene itself or those that regulate ACE2 function (i.e. SLC6A20) can alter this binding potential and thus the clinical impact of the virus. 

Aim 3:  Develop an integrated model of non-genomic (Aim 1) and genomic (Aim 2) factors for prediction of the three potential clinical courses of an individual upon exposure to SARS-CoV-2.  

Hypothesis:  An integrated model incorporating quantitative analysis of cytokines/immune cells (Aim 1) and gene sequence analysis (Aim 2) will allow a more robust and accurate prediction for one of the three potential clinical courses (A, B, C) after SARS-CoV-2 exposure.