Circulating APP, NCAM and Aβ serve as biomarkers for Alzheimer’s disease

Chen, Keping; Gao, Tianli; Bai, Zhimao; Yuan, Ziming

doi:10.1016/j.brainres.2018.08.015

Cited by 11 publications

(9 citation statements)

References 21 publications

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“…Previous reports have demonstrated the association of miR‐219‐5p with the development of cancers, including hepatoma, glioblastoma, colorectal cancer, and gastric cancer . Different biomarkers such as lipid peroxidation, β2‐microglobulin, APP, neural cell adhesion molecule, Aβ, and circulating miR‐127‐3p have been found to be associated with the prognosis of patients with AD . In addition, miRNAs have been shown to play a vital role at posttranscriptional level in various physiological and pathological processes, and association of miRNAs with the development of AD have also been demonstrated.…”

Section: Discussionmentioning

confidence: 97%

“…[9][10][11]18 Different biomarkers such as lipid peroxidation, β2-microglobulin, APP, neural cell adhesion molecule, Aβ, and circulating miR-127-3p have been found to be associated with the prognosis of patients with AD. [19][20][21][22] In addition, miRNAs have been shown to play a vital role at posttranscriptional level in various physiological and pathological processes, 23 and association of miRNAs with the development of AD have also been demonstrated. For example, Xiong et al 24 found that knockdown of miR-124 improves AD-like phenotypes in mice through inhibiting 25 suggested that miR-15 targets BACE1, NFKB1, and IKK-α, and inhibits NF-κB signaling as well as Aβ accumulation.…”

Section: Discussionmentioning

confidence: 99%

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miR‐219‐5p inhibits tau phosphorylation by targeting TTBK1 and GSK‐3β in Alzheimer's disease

Chen

et al. 2018

J of Cellular Biochemistry

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As the most common neurodegenerative disease, Alzheimer's disease (AD) is characterized by memory, perception, and behavioral damage, which may ultimately lead to emotional fluctuation and even lethal delirium. Increasing studies indicate that microRNAs (miRNAs) are associated with pathological features of AD.However, the role of miR-219-5p in AD progression is still unclear. In this study, the functions of miR-219-5p were analyzed in vitro and in vivo. miR-219-5p was notably overexpressed in brain tissues of patients with AD. The overexpression of miR-219-5p activated the phosphorylation of Tau-Ser198, Tau-Ser199, Tau-Ser201, and Tau-Ser422. We further showed that miR-219-5p could mediate a decrease in the protein levels of tau-tubulin kinase 1 (TTBK1) and glycogen synthase kinase 3β (GSK-3β) by directly binding to their 3′-untranslated region, thereby promoting the phosphorylation of tau in SH-SY5Y Cells. Rescue experiments further revealed that the phosphorylation of tau-mediated by miR-219-5p was dependent on the inhibition of TTBK1 and GSK-3β. Moreover, suppressing the expression of both TTBK1 and GSK-3β using miR-219-5p remarkably rescued AD-like symptoms in amyloid precursor protein/presenilin 1 mice. Our findings indicate that the upregulation of TTBK1 and GSK-3β mediated by the loss of miR-219-5p is a possible mechanism that contributes to tau phosphorylation and AD progression.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

miR‐219‐5p inhibits tau phosphorylation by targeting TTBK1 and GSK‐3β in Alzheimer's disease

Chen

et al. 2018

J of Cellular Biochemistry

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“…In addition, a previous report using a distinct disease model (diabetic rat) found corresponding reductions in hippocampal GluA1 and NCAM expression levels that were accompanied by impaired synaptic currents mediated by the glutamatergic channels (34). Thus, beyond the alterations in adhesion molecules with links to AD and age‐related cognitive decline (17–20), the military blast‐induced changes in synaptic adhesion components may also be involved in the resulting disturbances in cognition and emotional behaviors.…”

Section: Discussionmentioning

confidence: 99%

“…Those synaptic markers decreased by RDX blasts have also been found reduced in Alzheimer's disease (AD) brains ( 16), thus we further addressed the hypothesis that blast shockwaves cause AD-type synaptic alterations by evaluating synaptic adhesion molecules with links to age-related synaptic decline and deficits in brains of those with AD (17)(18)(19)(20). We assessed neural cell adhesion molecule (NCAM) species, and the blast-exposed hippocampal explants exhibited selective vulnerability among them (Figure 3A).…”

Section: R E Su Lt Smentioning

confidence: 99%

Distinct and dementia‐related synaptopathy in the hippocampus after military blast exposures

et al. 2021

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Explosive shockwaves, and other types of blast exposures, are linked to injuries commonly associated with military service and to an increased risk for the onset of dementia. Neurological complications following a blast injury, including depression, anxiety, and memory problems, often persist even when brain damage is undetectable. Here, hippocampal explants were exposed to the explosive 1,3,5-trinitro-1,3,5-triazinane (RDX) to identify indicators of blast-induced changes within important neuronal circuitries. Highly controlled detonations of small, 1.7-gram RDX spherical charges reduced synaptic markers known to

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“…This glycoprotein plays important role in order to mediate adhesion and guidance during neuronal differentiation (Harley et al, 2018). Studies have reported that NCAM could be altered in Alzheimer patients and could be used as desirable biomarker of this disease (Chen, Gao, Bai, & Yuan, 2018).…”

Section: Introductionmentioning

confidence: 99%

Elevated levels of BDNF and cathepsin‐das possible peripheral markers of neurodegeneration in plasma of patients with glutaric acidemia type I

Guerreiro

Jaques

Wajner

et al. 2020

Intl J of Devlp Neuroscience

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Glutaric acidemia type I (GA1) is caused by severe deficiency of glutaryl‐CoA dehydrogenase activity, resulting in an accumulation of glutaric acid and glutarylcarnitine (C5DC) in the organism. Patients affected by GA1 are asymptomatic in the neonate period but usually manifest chronically progressive neurodegeneration apart from severe encephalopathic crises associated with acute striatum necrosis. Neurological manifestations like dyskinesia, dystonia, hypotonia, muscle stiffness, and spasticity are present. Treatment is based on protein/lysine restriction and l‐carnitine supplementation. In this work, we evaluated markers of neurodegeneration and inflammation, namely BDNF (brain‐derived neurotrophic factor), NCAM (neuronal adhesion molecule), PDGF‐AA (platelet‐derived growth factor), and cathepsin‐d in plasma of six treated GA1 patients. We first found marked increases of plasma C5DC concentrations in GA1 patients, as well as increased levels of the markers BDNF and cathepsin‐d as compared to those of age‐matched healthy children. Furthermore, C5DC concentrations were highly correlated with the levels of cathepsin‐d. These results may demonstrate that brain tissue degeneration is present in GA1 patients and that there is a relationship between increased metabolites concentrations with this process. To the best of our knowledge, this is so far the first study showing altered peripheral parameters of neurodegeneration and inflammation in GA1 patients.

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Circulating APP, NCAM and Aβ serve as biomarkers for Alzheimer’s disease

Cited by 11 publications

References 21 publications

miR‐219‐5p inhibits tau phosphorylation by targeting TTBK1 and GSK‐3β in Alzheimer's disease

miR‐219‐5p inhibits tau phosphorylation by targeting TTBK1 and GSK‐3β in Alzheimer's disease

Distinct and dementia‐related synaptopathy in the hippocampus after military blast exposures

Elevated levels of BDNF and cathepsin‐das possible peripheral markers of neurodegeneration in plasma of patients with glutaric acidemia type I

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