Neurogenin 2 Mediates Amyloid-β Precursor Protein-stimulated Neurogenesis

Bolós, Marta; Hu, Yanling; Young, Karen; Foa, Lisa; Small, David H.

doi:10.1074/jbc.m114.581918

Cited by 21 publications

(9 citation statements)

References 63 publications

(73 reference statements)

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“…NGN2 also specifies phenotypic features of neurons and regulates axonal guidance ( 29 ). NGN2 has been found to correlate with APP expression by an increase in APP transgenic mice (Tg2576) but significantly down-regulated in neural stem/progenitor cells from APP knockout mice ( 30 ). In addition, a close relationship between NGN2 and APP was found in our study, but the origin of our NGN2 expression is unclear as limited information is available about peripheral NGN2.…”

Section: Discussionmentioning

confidence: 99%

A plasma protein classifier for predicting amyloid burden for preclinical Alzheimer’s disease

et al. 2019

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Section: Discussionmentioning

confidence: 99%

A plasma protein classifier for predicting amyloid burden for preclinical Alzheimer’s disease

et al. 2019

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“…In addition, APP770 contains an OX2 domain following the KPI domain. APP plays numerous functions, such as neuronal differentiation, neurogenesis, synaptic function, apoptosis and cell proliferation (Bolós et al, 2014 ; Milosch et al, 2014 ; Fanutza et al, 2015 ; Wu et al, 2015 , 2016 ).…”

Section: App Gene and Proteinmentioning

confidence: 99%

Modifications and Trafficking of APP in the Pathogenesis of Alzheimer’s Disease

Wang

Zhou

et al. 2017

Front. Mol. Neurosci.

120

102

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Alzheimer’s disease (AD), the most common neurodegenerative disorder, is the leading cause of dementia. Neuritic plaque, one of the major characteristics of AD neuropathology, mainly consists of amyloid β (Aβ) protein. Aβ is derived from amyloid precursor protein (APP) by sequential cleavages of β- and γ-secretase. Although APP upregulation can promote AD pathogenesis by facilitating Aβ production, growing evidence indicates that aberrant post-translational modifications and trafficking of APP play a pivotal role in AD pathogenesis by dysregulating APP processing and Aβ generation. In this report, we reviewed the current knowledge of APP modifications and trafficking as well as their role in APP processing. More importantly, we discussed the effect of aberrant APP modifications and trafficking on Aβ generation and the underlying mechanisms, which may provide novel strategies for drug development in AD.

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“…The expression of CBFA2T3, NEUROG2 (OMIM*606624) and ASCL1 (OMIM*100790) genes overlapped, and transcription assay showed that NEUROG2 and ASCL1 are inhibited by the MTG protein family, in which the CBFA2T3 gene was the most efficient to inhibit the transcription activity [27]. The proneural factor NEUROG2 mediates APP -stimulated neuronal differentiation of neural stem/progenitor cells ( NSPCs ) to neurons, and levels of NEUROG2 are correlated with amyloid-precursor protein ( APP ) expression [28], which means that rare mutations of CBFA2T3 might influence the APP expression. APP is a single-pass transmembrane protein expressed at high levels in the brain, and the generation and accumulation of Aβ 42 from sequential APP proteolysis is the crucial step in the development of AD [29].…”

Section: Resultsmentioning

confidence: 99%

Genome-wide association study identifies CBFA2T3 affecting the rate of CSF Aβ42 decline in non-demented elders

Dou

Zhang

Tan

et al. 2019

Aging

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Brain amyloid deposition is an early pathological event in Alzheimer’s disease (AD), and abnormally low levels amyloid-β 42 peptide (Aβ 42 ) in cerebrospinal fluid (CSF) can be detected in preclinical AD. To identify the genetic determinants that regulate the rate of CSF Aβ 42 decline among non-demented elders, we conducted a genome-wide association study involved 321 non-demented elders from Alzheimer’s Disease Neuroimaging Initiative (ADNI) 1/GO/2 cohorts restricted to non-Hispanic Caucasians. A novel genome-wide significant association of higher annualized percent decline of CSF Aβ 42 in the gene CBFA2T3 ( CBFA2/RUNX1 translocation partner 3; rs13333659-T; p = 2.24 × 10 −9 ) was identified. Besides displaying abnormal CSF Aβ 42 levels, rs13333659-T carriers were more likely to exhibit a greater longitudinal cognitive decline ( p = 0.029, β = 0.097) and hippocampal atrophy ( p = 0.029, β = −0.160) in the non-demented elders, especially for the participants who were amyloid-positive at baseline. These findings suggest rs13333659 in CBFA2T3 as a risk locus to modulate the decline rate of CSF Aβ 42 preceding the onset of clinical symptoms.

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Neurogenin 2 Mediates Amyloid-β Precursor Protein-stimulated Neurogenesis

Cited by 21 publications

References 63 publications

A plasma protein classifier for predicting amyloid burden for preclinical Alzheimer’s disease

A plasma protein classifier for predicting amyloid burden for preclinical Alzheimer’s disease

Modifications and Trafficking of APP in the Pathogenesis of Alzheimer’s Disease

Genome-wide association study identifies CBFA2T3 affecting the rate of CSF Aβ42 decline in non-demented elders

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