scholarly journals Is Cerebrospinal Fluid Superoxide Dismutase 1 a Biomarker of Tau But Not Amyloid-Induced Neurodegeneration in Alzheimer's Disease?

2019 ◽  
Vol 31 (8) ◽  
pp. 572-578 ◽  
Author(s):  
Kelsey E. McLimans ◽  
Bridget E. Clark ◽  
Alexandra Plagman ◽  
Colleen Pappas ◽  
Brandon Klinedinst ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Superoxide Dismutase ◽  
Superoxide Dismutase 1

scholarly journals S-Adenosylmethionine and Superoxide Dismutase 1 Synergistically Counteract Alzheimer’s Disease Features Progression in TgCRND8 Mice

Antioxidants ◽  
2017 ◽  
Vol 6 (4) ◽  
pp. 76 ◽  
Author(s):  
Rosaria Cavallaro ◽  
Vincenzina Nicolia ◽  
Maria Fiorenza ◽  
Sigfrido Scarpa ◽  
Andrea Fuso
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Superoxide Dismutase ◽  
Superoxide Dismutase 1 ◽  
Tgcrnd8 Mice

scholarly journals P3-233: ASSOCIATIONS OF CSF SUPEROXIDE DISMUTASE 1 WITH COGNITIVE, NEURAL, AND CSF BIOMARKERS ACROSS THE ALZHEIMER'S DISEASE SPECTRUM

2019 ◽  
Vol 15 ◽  
pp. P1022-P1022
Author(s):  
Kelsey E. McLimans ◽  
Bridget Clark ◽  
Colleen Pappas ◽  
Alexandra K. Plagman ◽  
Tovah Wolf ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Superoxide Dismutase ◽  
Csf Biomarkers ◽  
Superoxide Dismutase 1 ◽  
Disease Spectrum

P3-378: Misfolded superoxide dismutase 1 (SOD1) as a novel target for Alzheimer's disease

2010 ◽  
Vol 6 ◽  
pp. S563-S563
Author(s):  
Leslie I. Grad ◽  
James Donkin ◽  
Megan A. O'Neill ◽  
Jing Wang ◽  
Louise A. Scrocchi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Superoxide Dismutase ◽  
Superoxide Dismutase 1 ◽  
Novel Target

Amyloid beta in the Cerebrospinal Fluid and the Blood as a Biomarker for Alzheimer's Disease

HAPS Educator ◽  
2015 ◽  
Vol 20 (1) ◽  
pp. 38-43
Author(s):  
Brie Paddock ◽  
Kimberly Canfield ◽  
Sarah Cooper
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Amyloid Beta

scholarly journals On the design of early-phase Alzheimer’s disease clinical trials with cerebrospinal fluid tau outcomes

2021 ◽  
pp. 174077452110344
Author(s):  
Michelle M Nuño ◽  
Joshua D Grill ◽  
Daniel L Gillen ◽  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Clinical Trials ◽  
Cerebrospinal Fluid ◽  
Phosphorylated Tau ◽  
Inclusion Criteria ◽  
Eligibility Criteria ◽  
Total Tau ◽  
Prodromal Alzheimer’S Disease ◽  
Study Power

Background/Aims: The focus of Alzheimer’s disease studies has shifted to earlier disease stages, including mild cognitive impairment. Biomarker inclusion criteria are often incorporated into mild cognitive impairment clinical trials to identify individuals with “prodromal Alzheimer’s disease” to ensure appropriate drug targets and enrich for participants likely to develop Alzheimer’s disease dementia. The use of these eligibility criteria may affect study power. Methods: We investigated outcome variability and study power in the setting of proof-of-concept prodromal Alzheimer’s disease trials that incorporate cerebrospinal fluid levels of total tau (t-tau) and phosphorylated (p-tau) as primary outcomes and how differing biomarker inclusion criteria affect power. We used data from the Alzheimer’s Disease Neuroimaging Initiative to model trial scenarios and to estimate the variance and within-subject correlation of total and phosphorylated tau. These estimates were then used to investigate the differences in study power for trials considering these two surrogate outcomes. Results: Patient characteristics were similar for all eligibility criteria. The lowest outcome variance and highest within-subject correlation were obtained when phosphorylated tau was used as an eligibility criterion, compared to amyloid beta or total tau, regardless of whether total tau or phosphorylated tau were used as primary outcomes. Power increased when eligibility criteria were broadened to allow for enrollment of subjects with either low amyloid beta or high phosphorylated tau. Conclusion: Specific biomarker inclusion criteria may impact statistical power in trials using total tau or phosphorylated tau as the primary outcome. In concert with other important considerations such as treatment target and population of clinical interest, these results may have implications to the integrity and efficiency of prodromal Alzheimer’s disease trial designs.

scholarly journals “Don’t Phos Over Tau”: recent developments in clinical biomarkers and therapies targeting tau phosphorylation in Alzheimer’s disease and other tauopathies

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Yuxing Xia ◽  
Stefan Prokop ◽  
Benoit I. Giasson
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Kinase Inhibitors ◽  
Tau Phosphorylation ◽  
Phosphorylated Tau ◽  
Clinical Biomarkers ◽  
Early Results ◽  
Recent Developments ◽  
Tau Aggregation

AbstractPhosphorylation is one of the most prevalent post-translational modifications found in aggregated tau isolated from Alzheimer’s disease (AD) patient brains. In tauopathies like AD, increased phosphorylation or hyperphosphorylation can contribute to microtubule dysfunction and is associated with tau aggregation. In this review, we provide an overview of the structure and functions of tau protein as well as the physiologic roles of tau phosphorylation. We also extensively survey tau phosphorylation sites identified in brain tissue and cerebrospinal fluid from AD patients compared to age-matched healthy controls, which may serve as disease-specific biomarkers. Recently, new assays have been developed to measure minute amounts of specific forms of phosphorylated tau in both cerebrospinal fluid and plasma, which could potentially be useful for aiding clinical diagnosis and monitoring disease progression. Additionally, multiple therapies targeting phosphorylated tau are in various stages of clinical trials including kinase inhibitors, phosphatase activators, and tau immunotherapy. With promising early results, therapies that target phosphorylated tau  could be useful at slowing tau hyperphosphorylation and aggregation in AD and other tauopathies.

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