The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Dysregulation of the Retromer Complex System in Down Syndrome
Abstract
Objective: Most of the patients with Down syndrome (DS) develop Alzheimer's disease (AD) neuropathology by age 40. Although this increased susceptibility to AD in DS is thought to be primarily due to triplication of the amyloid precursor protein located on chromosome 21, the precise molecular mechanisms are not well understood. Recent evidence has implicated defective protein sorting and trafficking secondary to deficiencies in retromer complex proteins in AD pathogenesis. Thus, the objective of the present study is to assess the retromer complex system in DS. Methods: Human postmortem brain tissue and fibroblasts from subjects with DS and healthy controls were examined for the various retromer protein components using Western blot analysis and reverse transcription quantitative polymerase chain reaction (RT‐qPCR). Results: Retromer recognition core proteins were significantly decreased in DS fibroblasts, and in both the hippocampi and cortices of young (age 15–40 years old) and aged (40–65 years old) subjects with DS compared with controls. Correlation analyses showed a significant inverse relationship between recognition core proteins and levels of soluble forms of Aβ 1–40 and 1–42 in both hippocampus (n = 33, Spearman = −0.59 to −0.38, p ≤ 0.03 for VPS35, VPS26, VPS29, and VPS26B) and cortex tissue (n = 57, Spearman = −0.46 to −0.27, p ≤ 0.04 for VPS35, VPS26, and VPS29) of the same patients. Interpretation: We conclude that dysregulation of the retromer complex system is an early event in the development of the AD‐like pathology and cognitive decline in DS, and for this reason the system could represent a novel potential therapeutic target for DS. ANN NEUROL 2020 ANN NEUROL 2020;88:137–147
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Retromer complex protein levels inversely correlate with Alzheimer's disease-like neuropathology in Down syndrome subjects.
“Retromer complex proteins are decreased in postmortem brain tissues from Down syndrome subjects and inversely correlate with the Alzheimer’s disease-like neuropathology.”
From Retromer Stabilization Improves Cognitive Function and Synaptic Plasticity in a Mouse Model of Down Syndrome (2023) · cites this paper as [10]
Retromer complex proteins are decreased in postmortem brain tissues from Down syndrome subjects.
“Retromer complex proteins are decreased in postmortem brain tissues from Down syndrome subjects and inversely correlate with the Alzheimer’s disease-like neuropathology.”
From Retromer Stabilization Improves Cognitive Function and Synaptic Plasticity in a Mouse Model of Down Syndrome (2023) · cites this paper as [10]
Retromer complex proteins are reduced in induced pluripotent stem cell (iPSC)-derived neurons from subjects with Down syndrome.
“We previously showed that the retromer complex proteins are also reduced in postmortem brain tissues and induced pluripotent stem cell (iPSC) derived neurons from subjects with DS [9, 10].”
From Retromer Stabilization Improves Cognitive Function and Synaptic Plasticity in a Mouse Model of Down Syndrome (2023) · cites this paper as [10]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Cawley, S., Bekiranov, S., Ng, H. H., Kapranov, P., Sekinger, E. A., Kampa, D., Piccolboni, A., Sementchenko, V., Cheng, J., Williams, A. J., et al. (2004) · Cell · doi:10.1016/s0092-8674(04)00127-8 · Cited by 1,095
Down syndrome and Alzheimer's disease: common pathways, common goals
Hartley, D., Blumenthal, T., Carrillo, M., DiPaolo, G., Esralew, L., Gardiner, K., Granholm, A.-C., Iqbal, K., Krams, M., Lemere, C., et al. (2015) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2014.10.007 · Cited by 290
VPS35 haploinsufficiency increases Alzheimer’s disease neuropathology
Wen, L., Tang, F.-L., Hong, Y., Luo, S.-W., Wang, C.-L., He, W., Shen, C., Jung, J.-U., Xiong, F., Lee, D.-H., et al. (2011) · Journal of Cell Biology · doi:10.1083/jcb.201105109 · Cited by 270
Muhammad, A., Flores, I., Zhang, H., Yu, R., Staniszewski, A., Planel, E., Herman, M., Ho, L., Kreber, R., Honig, L. S., et al. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0802545105 · Cited by 248
Trisomy of human chromosome 21 enhances amyloid-β deposition independently of an extra copy of APP
Wiseman, F. K., Pulford, L. J., Barkus, C., Liao, F., Portelius, E., Webb, R., Chávez-Gutiérrez, L., Cleverley, K., Noy, S., Sheppard, O., et al. (2018) · Brain · doi:10.1093/brain/awy159 · Cited by 133
Flagged first, then by citations
Research works printed but not linked: 23
- 10.1002/alz.12068 · DOI · Paper page
- 10.1016/S0002-9440(10)64538-5 · DOI · Paper page
- 10.2353/ajpath.2008.071053 · DOI
- 10.1016/j.neurobiolaging.2004.02.027 · DOI · Paper page
- 10.1002/ana.20667 · DOI · Paper page
- 10.1038/mp.2015.121 · DOI · Paper page
- 10.1016/j.neurobiolaging.2012.04.020 · DOI · Paper page
- 10.1038/s41380-018-0221-3 · DOI · Paper page
- 10.1016/j.nbd.2012.03.030 · DOI · Paper page
- 10.1038/s41380-019-0364-x · DOI
- 10.1038/mp.2015.78 · DOI
- 10.1002/ana.24145 · DOI
- 10.1111/acel.12550 · DOI
- Head E, 2012, Alzheimer's disease in down syndrome, Eur J Neurodegener Dis, 1, 353
- 10.1038/nrn3896 · DOI · Paper page
- 10.1016/j.ajhg.2011.06.001 · DOI · Paper page
- 10.1038/ng.2802 · DOI · Paper page
- 10.1186/1866-1955-5-19 · DOI
- 10.1002/ajmg.c.30098 · DOI
- Bras A, 2018, Down syndrome and microRNAs, Biomed Rep, 8, 11
- 10.1038/nrg1448 · DOI · Paper page
- 10.1016/j.stemcr.2018.01.031 · DOI · Paper page
- 10.1186/s13024-019-0350-4 · DOI · Paper page
Cited by
Sorted by citations
Wu, Y., Mumford, P., Noy, S., Cleverley, K., Mrzyglod, A., Luo, D., van Dalen, F., Verdoes, M., Fisher, E. M. C., & Wiseman, F. K. (2023) · Acta Neuropathologica Communications · doi:10.1186/s40478-023-01632-8 · Cited by 16
Curtis, M. E., Smith, T., Nenov, M., Blass, B. E., & Praticò, D. (2023) · Journal of Alzheimer's Disease · doi:10.3233/jad-230205 · Cited by 3
Self-citation
Metadata
- Authors
- Curtis, M. E., Yu, D., & Praticò, D.
- Affiliations
- Alzheimer's Center at Temple Temple University Lewis Katz School of Medicine Philadelphia PA USA
- Department of Clinical Sciences Temple University Lewis Katz School of Medicine Philadelphia PA USA
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 2020-05-27
- Volume
- 88
- Issue
- 1
- Pages
- 137-147
- ISSN
- 0364-5134
- 1531-8249
- PMC
- PMC7384049
- Cited by
- 29
- References
- 5
- Language
- en
- Funders
- National Institute on Aging (AG055707, AG056689)
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
