Correlations of amyloid-β concentrations between CSF and plasma in acute Alzheimer mouse model

Cho, Soo Min; Kim, Hyunjin Vincent; Lee, Se-Jin; Kim, Hye Yun; Kim, Woong; Kim, Tae Song; Kim, Dong Jin; Kim, Young Soo

doi:10.1038/srep06777

Cited by 36 publications

(36 citation statements)

References 24 publications

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“…Nutriproteomic diets as a treatment for reduction of LPS effects may lower TSP-1 expression by peripheral cells [190,191,192] and improve peripheral LPS–protein interactions [193,194,195,196] to accelerate peripheral amyloid beta metabolism with respect to treatment of individuals with prodromal disease and dementia. Nutritional diets that activate Sirt 1 and maintain therapeutic VIP and FGF21 levels [51] accelerate hepatic LPS/mycotoxin metabolism without transfer to the CSF and brain compartment [21], which is consistent with the use of nutritional therapy to maintain CSF composition, recycling, and amyloid beta dynamics [197,198] for the prevention of early neurodegeneration (stages 1–3) and amyloidosis.…”

Section: Nutriproteomic Diets Regulates Plasma Biomarkers and Revementioning

confidence: 66%

The Role of Clinical Proteomics, Lipidomics, and Genomics in the Diagnosis of Alzheimer’s Disease

Martins

2016

Proteomes

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The early diagnosis of Alzheimer’s disease (AD) has become important to the reversal and treatment of neurodegeneration, which may be relevant to premature brain aging that is associated with chronic disease progression. Clinical proteomics allows the detection of various proteins in fluids such as the urine, plasma, and cerebrospinal fluid for the diagnosis of AD. Interest in lipidomics has accelerated with plasma testing for various lipid biomarkers that may with clinical proteomics provide a more reproducible diagnosis for early brain aging that is connected to other chronic diseases. The combination of proteomics with lipidomics may decrease the biological variability between studies and provide reproducible results that detect a community’s susceptibility to AD. The diagnosis of chronic disease associated with AD that now involves genomics may provide increased sensitivity to avoid inadvertent errors related to plasma versus cerebrospinal fluid testing by proteomics and lipidomics that identify new disease biomarkers in body fluids, cells, and tissues. The diagnosis of AD by various plasma biomarkers with clinical proteomics may now require the involvement of lipidomics and genomics to provide interpretation of proteomic results from various laboratories around the world.

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Section: Nutriproteomic Diets Regulates Plasma Biomarkers and Revementioning

confidence: 66%

The Role of Clinical Proteomics, Lipidomics, and Genomics in the Diagnosis of Alzheimer’s Disease

Martins

2016

Proteomes

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“…Ideal surrogate biomarkers would be accessible, affordable, and abundant so that they could be implemented into pointof-care testing and thus allow the reliable diagnosis of atrisk patients. Studies dedicated to establishing biomarkers obtained from CSF, blood, and other bodily fluids have demonstrated the individual potential of these biomarkers ( Table 1) and have delineated the correlations between AD and the biomarkers obtained from differing fluids 88,89 . Most research pertaining to these varying biomarkers utilizes similar methodologies despite the difference in fluid mediums.…”

Section: Seldi-ms Protein Array Chipmentioning

confidence: 99%

Diagnosis of Alzheimer’s disease utilizing amyloid and tau as fluid biomarkers

et al. 2019

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Current technological advancements in clinical and research settings have permitted a more intensive and comprehensive understanding of Alzheimer’s disease (AD). This development in knowledge regarding AD pathogenesis has been implemented to produce disease-modifying drugs. The potential for accessible and effective therapeutic methods has generated a need for detecting this neurodegenerative disorder during early stages of progression because such remedial effects are more profound when implemented during the initial, prolonged prodromal stages of pathogenesis. The aggregation of amyloid-β (Aβ) and tau isoforms are characteristic of AD; thus, they are considered core candidate biomarkers. However, research attempting to establish the reliability of Aβ and tau as biomarkers has culminated in an amalgamation of contradictory results and theories regarding the biomarker concentrations necessary for an accurate diagnosis. In this review, we consider the capabilities and limitations of fluid biomarkers collected from cerebrospinal fluid, blood, and oral, ocular, and olfactory secretions as diagnostic tools for AD, along with the impact of the integration of these biomarkers in clinical settings. Furthermore, the evolution of diagnostic criteria and novel research findings are discussed. This review is a summary and reflection of the ongoing concerted efforts to establish fluid biomarkers as a diagnostic tool and implement them in diagnostic procedures.

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“…Previously, we have illustrated that cBMECs were used as a cellular index of the BBB damage caused by microbial ( E. coli K1 and gp120) and non-microbial (nicotine and METH) pathogenic insults11. Leakage of peripheral proteins into the CNS has been used to evaluate BBB permeability3132, such as fibrinogen or albumin. There are a number of peripheral blood biomarkers for detection of BBB injury, including UCHL1, RAGE and its ligand S100B.…”

Section: Disscussionmentioning

confidence: 99%

Alpha7 nicotinic acetylcholine receptor is required for amyloid pathology in brain endothelial cells induced by Glycoprotein 120, methamphetamine and nicotine

Liu

et al. 2017

Sci Rep

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One of the most challenging issues in HIV-associated neurocognitive disorders (HAND) caused by HIV-1 virotoxins and drug abuse is the lack of understanding the underlying mechanisms that are commonly associated with disorders of the blood-brain barrier (BBB), which mainly consists of brain microvascular endothelial cells (BMEC). Here, we hypothesized that Glycoprotein 120 (gp120), methamphetamine (METH) and nicotine (NT) can enhance amyloid-beta (Aβ) accumulation in BMEC through Alpha7 nicotinic acetylcholine receptor (α7 nAChR). Both in vitro (human BMEC) (HBMEC) and in vivo (mice) models of BBB were used to dissect the role of α7 nAChR in up-regulation of Aβ induced by gp120, METH and NT. Aβ release from and transport across HBMEC were significantly increased by these factors. Methyllycaconitine (MLA), an antagonist of α7 nAChR, could efficiently block these pathogenic effects. Furthermore, our animal data showed that these factors could significantly increase the levels of Aβ, Tau and Ubiquitin C-Terminal Hydrolase L1 (UCHL1) in mouse cerebrospinal fluid (CSF) and Aβ in the mouse brains. These pathogenicities were significantly reduced by MLA, suggesting that α7 nAChR may play an important role in neuropathology caused by gp120, METH and NT, which are the major pathogenic factors contributing to the pathogenesis of HAND.

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Correlations of amyloid-β concentrations between CSF and plasma in acute Alzheimer mouse model

Cited by 36 publications

References 24 publications

The Role of Clinical Proteomics, Lipidomics, and Genomics in the Diagnosis of Alzheimer’s Disease

The Role of Clinical Proteomics, Lipidomics, and Genomics in the Diagnosis of Alzheimer’s Disease

Diagnosis of Alzheimer’s disease utilizing amyloid and tau as fluid biomarkers

Alpha7 nicotinic acetylcholine receptor is required for amyloid pathology in brain endothelial cells induced by Glycoprotein 120, methamphetamine and nicotine

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