Plasma long non-coding RNA BACE1 as a novel biomarker for diagnosis of Alzheimer disease

Feng, Liang; Liao, Yuting; He, Jincai; Xie, Cheng-Long; Chen, Siyan; Fan, Huihui; Su, Zhipeng; Wang, Zhen

doi:10.1186/s12883-017-1008-x

Cited by 117 publications

(101 citation statements)

References 40 publications

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“…This leads to the production of more Aβ 42 and an increase in the formation of SPs in the brain in AD patients, aggravating the development of the disease. Feng et al found that the level of the BACE1 is increased in the plasma of AD patients and that it has a high specificity (88%) for AD, indicating BACE1 may be a potential candidate biomarker to predict AD (Feng et al, 2018 ). Recently, Yang et al, investigated the hippocampal expression patterns of dysregulated lncRNAs in a rat model of AD through microarray (Yang et al, 2017 ).…”

Section: The Role Of Lncrnas In Neurodegenerative Diseasesmentioning

confidence: 99%

The Role of Long Noncoding RNAs in Central Nervous System and Neurodegenerative Diseases

Wei¹,

Luo²,

Zou³

et al. 2018

Front. Behav. Neurosci.

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Long noncoding RNAs (lncRNAs) refer to a group of noncoding RNAs (ncRNAs) that has a transcript of more than 200 nucleotides in length in eukaryotic cells. The lncRNAs regulate gene expression at epigenetic, transcriptional, and post-transcriptional levels by multiple action modes. In this review, we describe the diverse roles reported for lncRNAs, and discuss how they could mechanistically be involved in the development of central nervous system (CNS) and neurodegenerative diseases. Further studies on the function of lncRNAs and their mechanism will help deepen our understanding of the development, function, and diseases of the CNS, and provide new ideas for the design and development of some therapeutic drugs.

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Section: The Role Of Lncrnas In Neurodegenerative Diseasesmentioning

confidence: 99%

The Role of Long Noncoding RNAs in Central Nervous System and Neurodegenerative Diseases

Wei¹,

Luo²,

Zou³

et al. 2018

Front. Behav. Neurosci.

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“…Upregulation of BC200 promotes BACE-1 activity and plasticity failure in AD postmortem brain tissues. Moreover, BC200 upregulation potentiates Aβ42 expression via a direct promotion of BACE-1 expression and subsequent impairment of cell viability [84][85][86]. The level of neuroblastoma differentiation marker 29 (NDM29) is increased by inflammation.…”

Section: Ncrnas In the Regulation Of Aβ Generation And Accumulationmentioning

confidence: 99%

“…In AD patient brains, NDM29 upregulation induces APP synthesis and promotes its cleavage by BACE1 and γ-secretase. Upregulation of BC200 or NDM29 increase Aβ secretion and the Aβ42/40 ratio [85,86]. BACE1-AS is a conserved RNA transcribed from the opposite strand of the BACE1 locus on chromosome 11 (11q23).…”

Section: Ncrnas In the Regulation Of Aβ Generation And Accumulationmentioning

confidence: 99%

Functional roles and networks of non-coding RNAs in the pathogenesis of neurodegenerative diseases

2020

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Recent transcriptome analyses have revealed that noncoding RNAs (ncRNAs) are broadly expressed in mammalian cells and abundant in the CNS, with tissue and cell type-specific expression patterns. Moreover, ncRNAs have been found to intricately and dynamically regulate various signaling pathways in neurodegeneration. As such, some antisense transcripts and microRNAs are known to directly affect neurodegeneration in disease contexts. The functions of ncRNAs in pathogenesis are unique for each disorder, as are the pertinent networks of ncRNA/miRNA/ mRNA that mediate these functions. Thus, further understanding of ncRNA biogenesis and effects might aid the discovery of diagnostic biomarkers or development of effective therapeutics for neurodegenerative disorders. Here, we review the ncRNAs that have so far been identified in major neurodegenerative disease etiology and the mechanisms that link ncRNAs with disease-specific phenotypes, such as HTT aggregation in HD, α-synuclein in PD, and Aβ plaques and hyperphosphorylated Tau in AD. We also summarize the known lncRNA/miRNA/mRNA networks that participate in neurodegenerative diseases, and we discuss ncRNA-related treatments shown to delay disease onset and prolong lifespan in rodent models.

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“…Altered lncRNA transcription may be involved in increasing the risk of AD. There is evidence for several specific lncRNAs being dysregulated in AD, including APP, and BACE1 [128]. Such altered expression is detectable not only in AD brain, but also in the plasma and CSF of these patients [128][129][130][131].…”

Section: Long Non-coding Rnas (Lnc-rnas)mentioning

confidence: 99%

“…There is evidence for several specific lncRNAs being dysregulated in AD, including APP, and BACE1 [128]. Such altered expression is detectable not only in AD brain, but also in the plasma and CSF of these patients [128][129][130][131]. In particular, BACE1-AS lncRNA is an antisense RNA transcribed by RNA polymerase II from the complementary strand of BACE1 in the locus 11q 23.3 [132]; it is directly implicated in the increased abundance of Aβ 1-42 in AD.…”

Section: Long Non-coding Rnas (Lnc-rnas)mentioning

confidence: 99%

Neuroepigenetics and Alzheimer’s Disease: An Update

Zusso

Barbierato

Facci

et al. 2018

JAD

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Epigenetics is the study of changes in gene expression which may be triggered by both genetic and environmental factors, and independent from changes to the underlying DNA sequence-a change in phenotype without a change in genotype-which in turn affects how cells read genes. Epigenetic changes represent a regular and natural occurrence but can be influenced also by factors such as age, environment, and disease state. Epigenetic modifications can manifest themselves not only as the manner in which cells terminally differentiate, but can have also deleterious effects, resulting in diseases such as cancer. At least three systems including DNA methylation, histone modification, and non-coding RNA (ncRNA)-associated gene silencing are thought to initiate and sustain epigenetic change. For example, in Alzheimer's disease (AD), both genetic and non-genetic factors contribute to disease etiopathology. While over 250 gene mutations have been related to familial AD, less than 5% of AD cases are explained by known disease genes. More than likely, non-genetic factors, probably triggered by environmental factors, are causative factors of late-onset AD. AD is associated with dysregulation of DNA methylation, histone modifications, and ncRNAs. Among the classes of ncRNA, microRNAs (miRNAs) have a well-established regulatory relevance. MicroRNAs are highly expressed in CNS neurons, where they play a major role in neuron differentiation, synaptogenesis, and plasticity. MicroRNAs impact higher cognitive functions, as their functional impairment is involved in the etiology of neurological diseases, including AD. Alterations in the miRNA network contribute to AD disease processes, e.g., in the regulation of amyloid peptides, tau, lipid metabolism, and neuroinflammation. MicroRNAs, both as biomarkers for AD and therapeutic targets, are in the early stages of exploration. In addition, emerging data suggest that altered transcription of long ncRNAs, endogenous, ncRNAs longer than 200 nucleotides, may be involved in an elevated risk for AD.

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Plasma long non-coding RNA BACE1 as a novel biomarker for diagnosis of Alzheimer disease

Cited by 117 publications

References 40 publications

The Role of Long Noncoding RNAs in Central Nervous System and Neurodegenerative Diseases

The Role of Long Noncoding RNAs in Central Nervous System and Neurodegenerative Diseases

Functional roles and networks of non-coding RNAs in the pathogenesis of neurodegenerative diseases

Neuroepigenetics and Alzheimer’s Disease: An Update

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