Abstract
Introduction. The amyloid cascade hypothesis proposes that extracellular senile plaques - largely composed of aggregated beta-amyloid (Aβ) peptides - are responsible for the events that lead to neuronal death that occurs in Alzheimer's disease (AD). On the other hand, the hyperphosphorylated (p-tau) and unstructured tau protein is responsible for intracellular neurofibrillary tangles, also common in AD. Clinical diagnostic criteria for AD include Aβ and p-tau biomarker tests in cerebrospinal fluid (CSF), in addition to neuroimaging measures, clinical history, and psychometric tests. However, due to their invasive nature, side effects and need for trained personnel in a hospital environment for their collection, CSF biomarkers are not suitable for large-scale screening. Therefore, alternative blood-based biomarkers are under intense investigation. Objective. Focus on recent advances in different p-tau isoforms as blood-based AD biomarkers. Method. Review performed by searches in Medline/PubMed databases. Results. The p-tau isoforms 181 and 217 represent accessible and scalable molecules for screening and diagnosing AD, mainly due to their ability to differentiate patients with the disease from cognitively healthy participants. These results should be reproduced in larger and more representative cohorts of population diversity. Conclusions. This review provides a more comprehensive exploration of blood p-tau as a specific molecular biomarker for AD, which could contribute not only to screening pre-symptomatic patients for clinical trials, but also to monitoring disease progression and evaluating modifying therapies. of the disease.
Highlights
The amyloid cascade hypothesis proposes that extracellular senile plaques largely composed of aggregated beta-amyloid (Aβ) peptides - are responsible for the events that lead to neuronal death that occurs in Alzheimer's disease (AD)
In a longitudinal cohort study that included data from blood sampling performed for up to 8 years, plasma ptau[181] and neurofilament light protein (NFL) measurements from 1113 participants, including cognitively unimpaired, as well as patients with mild cognitive impairment (MCI) and AD and measures and FDG-positron emission tomography (PET) or structural MRI scans showed that both p-tau[181] and NFL were independently associated with cognition and neurodegeneration in brain regions typically affected in AD
This review aimed to describe the recent advances on different p-tau isoforms as a blood-based biomarker for AD, provide a more comprehensive and detailed exploration of these biomarkers, and contribute to the advance of the literature on the theme
Summary
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the most common type of dementia worldwide, accounting for more than 60% of cases[1]. Extensive evidence indicates increased CSF p-tau in patients with AD compared to controls[16] and correlates with cognitive impairment better than Aβ-related biomarkers[43,44], being useful for disease staging and as a prognostic biomarker[45], accurately predicting progression from cognitively unimpaired to MCI and AD dementia[46]. In a longitudinal cohort study that included data from blood sampling performed for up to 8 years, plasma ptau[181] and NFL measurements from 1113 participants, including cognitively unimpaired, as well as patients with MCI and AD and measures and FDG-PET or structural MRI scans showed that both p-tau[181] and NFL were independently associated with cognition and neurodegeneration in brain regions typically affected in AD.
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