Changes of cerebrospinal fluid Aβ42, t-tau, and p-tau in Parkinson’s disease patients with cognitive impairment relative to those with normal cognition: a meta-analysis

Hu, Xiaohui; Yang, Yan; Gong, Daokai

doi:10.1007/s10072-017-3088-1

Cited by 49 publications

(34 citation statements)

References 34 publications

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“…For this study, results issued by the Welch's U -Test are consistent with the current state-of-the-art as reflected in Gallegos et al ( 2015 ), Klettner et al ( 2016 ), Xu et al ( 2017 ), Hu et al ( 2017 ), Vanle et al ( 2017 ), and Abbasi et al ( 2018 ), particulary for CSF and RNA tests ( CSF Alpha-synuclein , p- τ 181P , Total- τ, and GAPDH ). We confirm this hypothesis as we obtain better ensemble classification results when those biomarkers are included in our multimodal experiments.…”

Section: Discussionsupporting

confidence: 90%

Robust Ensemble Classification Methodology for I123-Ioflupane SPECT Images and Multiple Heterogeneous Biomarkers in the Diagnosis of Parkinson's Disease

Castillo-Barnes

Ramı́rez

Segovia

et al. 2018

Front. Neuroinform.

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In last years, several approaches to develop an effective Computer-Aided-Diagnosis (CAD) system for Parkinson's Disease (PD) have been proposed. Most of these methods have focused almost exclusively on brain images through the use of Machine-Learning algorithms suitable to characterize structural or functional patterns. Those patterns provide enough information about the status and/or the progression at intermediate and advanced stages of Parkinson's Disease. Nevertheless this information could be insufficient at early stages of the pathology. The Parkinson's Progression Markers Initiative (PPMI) database includes neurological images along with multiple biomedical tests. This information opens up the possibility of comparing different biomarker classification results. As data come from heterogeneous sources, it is expected that we could include some of these biomarkers in order to obtain new information about the pathology. Based on that idea, this work presents an Ensemble Classification model with Performance Weighting. This proposal has been tested comparing Healthy Control subjects (HC) vs. patients with PD (considering both PD and SWEDD labeled subjects as the same class). This model combines several Support-Vector-Machine (SVM) with linear kernel classifiers for different biomedical group of tests—including CerebroSpinal Fluid (CSF), RNA, and Serum tests—and pre-processed neuroimages features (Voxels-As-Features and a list of defined Morphological Features) from PPMI database subjects. The proposed methodology makes use of all data sources and selects the most discriminant features (mainly from neuroimages). Using this performance-weighted ensemble classification model, classification results up to 96% were obtained.

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Section: Discussionsupporting

confidence: 90%

Robust Ensemble Classification Methodology for I123-Ioflupane SPECT Images and Multiple Heterogeneous Biomarkers in the Diagnosis of Parkinson's Disease

Castillo-Barnes

Ramı́rez

Segovia

et al. 2018

Front. Neuroinform.

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“…In Parkinson's disease dementia (PDD) t-tau levels are also elevated compared controls or to Parkinson's disease patients with normal cognition, but lower than those detected in DLB [58,59]. Whether elevated levels of t-tau in PDD are related to an underlying tau pathology participating in the development of dementia, similar to AD, or just reflecting increased neuroaxonal damage compared to PD cases is still a matter of debate.…”

Section: Total Taumentioning

confidence: 99%

Tau Protein as a Biological Fluid Biomarker in Neurodegenerative Dementias

Llorens¹,

Villar‐Piqué²,

Candelise³

et al. 2019

Cognitive Disorders

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Tau is a microtubule-associated protein, whose main function is the modulation of the stability of axonal microtubules. In physiological conditions tau is abundant in neurons while its expression in glial populations is low and restricted to astrocytes and oligodendrocytes. The aggregation of tau in neurofibrillary or gliofibrillary tangles is the main hallmark of tauopathies, a complex group of human neurodegenerative conditions where tau hyper-phosphorylation causes its increased insolubility and aggregation leading to tangle formation and microtubule destabilization. Tau can be detected in biological fluids in physiological and pathological conditions. In several neurodegenerative dementias, either associated or not to a primary tauopathy, tau levels are altered in a diseasespecific pattern, which can be used as a biomarker for disease diagnosis and prognosis. The study of tau levels in biological fluids has been mainly performed in the cerebrospinal fluid (CSF), although the recent development of ultrasensitive techniques allows the robust quantification of tau in blood-based biofluids such as serum and plasma. The presence of elevated total-tau in the CSF is assumed to reflect the degree of axonal damage in the brain tissue. Consequently, highest total-tau CSF levels are found in sporadic Creutzfeldt-Jakob disease, which is characterized by massive neuronal damage and a rapid progressive course. Elevated total-tau is also detected in Alzheimer's disease and dementia with Lewy bodies, while in other dementia conditions such as vascular dementia, frontotemporal dementia and corticobasal degeneration are unchanged, inconclusive or not determined. Additionally, total-tau rises temporarily due to cerebral infarction. In contrast, elevated phospho-tau levels seem to be restricted to Alzheimer's disease pathology, most likely mirroring the presence of the hyper-phosphorylated form in the brain tissue, although phospho-tau levels are mainly unaffected in tauopathies. Additionally, isoforms and different structural and truncated tau forms have also been reported to be altered in neurodegenerative dementias. In this complex scenario the diagnostic accuracy of diverse tau forms as disease-specific biomarkers needs to be established. In this chapter, we summarize the current knowledge on the alterations of diverse tau forms

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“…This is further illustrated by neuronal phenotypes in knockout animal models of several different amyloid pathologies (Box 1). Moreover, in many amyloidopathies, the CSF levels of the soluble peptides/proteins that eventually form amyloid aggregates decrease rather than increase (Kang, 2016;Hu et al, 2017). In AD and PD, the decrease in CSF levels of soluble Aβ (Fagan et al, 2009;Bateman et al, 2012;Buchhave et al, 2012) and α-syn (Tokuda et al, 2006;Wang et al, 2015;Mollenhauer et al, 2019;Parnetti et al, 2019) is among the early biochemical markers of the disease.…”

Section: Gain or Loss Of Function?mentioning

confidence: 99%

Disentangling the Amyloid Pathways: A Mechanistic Approach to Etiology

et al. 2020

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Amyloids are fibrillar protein aggregates associated with diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), type II diabetes and Creutzfeldt-Jakob disease. The process of amyloid polymerization involves three pathological protein transformations; from natively folded conformation to the cross-β conformation, from biophysically soluble to insoluble, and from biologically functional to non-functional. While amyloids share a similar cross-β conformation, the biophysical transformation can either take place spontaneously via a homogeneous nucleation mechanism (HON) or catalytically on an exogenous surface via a heterogeneous nucleation mechanism (HEN). Here, we postulate that the different nucleation pathways can serve as a mechanistic basis for an etiological classification of amyloidopathies, where hereditary forms generally follow the HON pathway, while sporadic forms follow seed-induced (prions) or surface-induced (including microbially induced) HEN pathways. Critically, the conformational and biophysical amyloid transformation results in loss-of-function (LOF) of the original natively folded and soluble protein. This LOF can, at least initially, be the mechanism of amyloid toxicity even before amyloid accumulation reaches toxic levels. By highlighting the important role of non-protein species in amyloid formation and LOF mechanisms of toxicity, we propose a generalized mechanistic framework that could help better understand the diverse etiology of amyloid diseases and offer new opportunities for therapeutic interventions, including replacement therapies.

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Changes of cerebrospinal fluid Aβ42, t-tau, and p-tau in Parkinson’s disease patients with cognitive impairment relative to those with normal cognition: a meta-analysis

Cited by 49 publications

References 34 publications

Robust Ensemble Classification Methodology for I123-Ioflupane SPECT Images and Multiple Heterogeneous Biomarkers in the Diagnosis of Parkinson's Disease

Robust Ensemble Classification Methodology for I123-Ioflupane SPECT Images and Multiple Heterogeneous Biomarkers in the Diagnosis of Parkinson's Disease

Tau Protein as a Biological Fluid Biomarker in Neurodegenerative Dementias

Disentangling the Amyloid Pathways: A Mechanistic Approach to Etiology

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