Less than 50 years since tau was first isolated from a porcine brain, its detection in femtolitre concentrations in biological fluids is revolutionizing the diagnosis of neurodegenerative diseases. This review highlights the molecular and technological advances that have catapulted tau from obscurity to the forefront of biomarker diagnostics. Comprehensive updates are provided describing the burgeoning clinical applications of tau as a biomarker of neurodegeneration. For the clinician, tau not only enhances diagnostic accuracy, but holds promise as a predictor of clinical progression, phenotype, and response to drug therapy. For patients living with neurodegenerative disorders, characterization of tau dysregulation could provide much-needed clarity to a notoriously murky diagnostic landscape.
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http://dx.doi.org/10.3390/ijms23137307 | DOI Listing |
Nat Protoc
January 2025
Center for Nanoscience and Nanotechnology, Tel Aviv University, Tel Aviv-Yafo, Israel.
Nanostructured devices have proven useful in a broad range of applications, from diagnosing diseases to discovering and screening new drug molecules. We developed vertical silicon nanopillar (SiNP) arrays for on-chip multiplex capture of selected biomolecules using a light-induced release of the array's selectively captured biomarkers. This platform allows the rapid, reusable and quantitative capture and release of a selection of biomarkers, followed by their downstream analysis.
View Article and Find Full Text PDFBrain
January 2025
Translational Neuroimaging Laboratory, Montreal Neurological Institute, H3A 2B4, Montreal, Canada.
Plasma phosphorylated tau biomarkers open unprecedented opportunities for identifying carriers of Alzheimer's disease pathophysiology in early disease stages using minimally invasive techniques. Plasma p-tau biomarkers are believed to reflect tau phosphorylation and secretion. However, it remains unclear to what extent the magnitude of plasma p-tau abnormalities reflects neuronal network disturbance in the form of cognitive impairment.
View Article and Find Full Text PDFAlzheimers Dement
January 2025
Unitat de Trastorns Cognitius, Cognition and Behavior Study Group, Hospital Universitari Santa Maria Universitat de Lleida, Lleida, Spain.
Introduction: Changes in sleep physiology can predate cognitive symptoms by decades in persons with Alzheimer's disease (AD), but it remains unclear which sleep characteristics predict cognitive and neurodegenerative changes after AD onset.
Methods: Using data from a prospective cohort of mild to moderate AD (n = 60), we analyzed non-rapid eye movement sleep spindles and slow oscillations (SOs) at baseline and their associations with baseline amyloid beta (Aβ) and tau and with cognition from baseline to 3-year follow-up.
Results: Higher spindle and SO activity predicted significant changes in Aβ and tau at baseline, lower Alzheimer's Disease Assessment Scale Cognitive Subscale (better cognitive performance) score, and higher Mini-Mental State Examination score from baseline to 36 months.
Alzheimers Dement
January 2025
Department of Neurology, Neurological Institute, Taipei Veterans General Hospital, Taipei, Taiwan.
Introduction: Plasma phosphorylated tau (p-tau) biomarkers have improved Alzheimer's disease (AD) diagnosis, but data from diverse Asian populations are limited. This study evaluated plasma p-tau217 and p-tau181 levels in Korean and Taiwanese populations.
Methods: All participants (n = 270) underwent amyloid positron emission tomography (PET) and blood tests.
Background: Although Amyloid-beta and Tau are the hallmarks of Alzheimer's Disease (AD), other protein pathways such as endothelial dysfunction may be involved and may precede cognitive symptoms. Our objective was to characterize the cerebrospinal fluid (CSF) proteomic profiles focusing on cardiometabolic-related protein pathways in individuals on the AD spectrum.
Methods: We performed CSF and plasma-targeted proteomics (276 proteins) from 354 participants of the Brain Stress Hypertension and Aging Program (BSHARP), of which 8% had preclinical AD, and 24% had MCI due to AD.
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