The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
Beneficial Effect of a Small Pharmacologic Chaperone on the Established Alzheimer’s Disease Phenotype
Abstract
Background: The endosomal retromer complex system is a key controller for trafficking of proteins. Downregulation of its recognition core proteins, such as VPS35, is present in Alzheimer’s disease (AD) brain, whereas its normalization prevents the development of AD pathology in a transgenic model with amyloid-β deposits and tau tangles. Objective: Assess the effect of targeting VPS35 after the AD pathology and memory impairments have developed. Methods: Twelve-month-old triple transgenic mice were treated with a small pharmacological chaperone, TPT-172, or vehicle for 14 weeks. At the end of this period, the effect of the drug on their phenotype was evaluated. Results: While control mice had a decline of learning and memory, the group receiving the chaperone did not. Moreover, when compared with controls the treated mice had significantly less amyloid-β peptides and phosphorylated tau, elevation of post-synaptic protein, and reduction in astrocytes activation. Conclusion: Taken together, our findings demonstrate that pharmacologic stabilization of the retromer recognition core is beneficial also after the AD-like pathologic phenotype is established.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
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?
TPT-172 was previously shown to be effective in reducing in vivo classical Alzheimer's disease-like neuropathology in mice.
“Additionally, the same drug was previously shown to be effective in reducing in vivo the classical AD-like neuropathology in mice.”
From Retromer Stabilization Improves Cognitive Function and Synaptic Plasticity in a Mouse Model of Down Syndrome (2023) · cites this paper as [7]
Enhancing retromer function influences both amyloid and tau neuropathology in models of Alzheimer's disease.
“enhancing retromer function has been shown to influence both amyloid and tau neuropathology in models of the disease [7, 8].”
From Retromer Stabilization Improves Cognitive Function and Synaptic Plasticity in a Mouse Model of Down Syndrome (2023) · cites this paper as [7]
Our current results agree with previous studies in which TPT-172 was chronically administered to a mouse model of Alzheimer's disease with amyloid plaques and tangles (3xTg mice).
“Thus, our current results agree with our previous studies in which TPT-172 was chronically administered to a mouse model of AD with amyloid plaques and tangles, the 3xTg mice [7, 8].”
From Retromer Stabilization Improves Cognitive Function and Synaptic Plasticity in a Mouse Model of Down Syndrome (2023) · cites this paper as [7]
Citations
Cites
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
Flagged first, then by citations
Research works printed but not linked: 20
- Qureshi, 2020, Endosomal trafficking in Alzheimer’s disease, Parkinson’s disease, and neuronal ceroid lipofuscinosis, Mol Cell Biol, 40, e00262, 10.1128/MCB.00262-20 · DOI · Paper page
- Nixon, 2005, Endosome function and dysfunction in Alzheimer’s disease and other neurodegenerative diseases, Neurobiol Aging, 26, 373, 10.1016/j.neurobiolaging.2004.09.018 · DOI
- Kovtun, 2018, Structure of the membrane-assembled coat determined by cryo-electron tomography, Nature, 561, 561, 10.1038/s41586-018-0526-z · DOI · Paper page
- Seaman, 2021, The retromer complex: From genesis to revelations, Trends Biochem Sci, 46, 608, 10.1016/j.tibs.2020.12.009 · DOI · Paper page
- Vagnozzi, 2019, Endosomal sorting and trafficking, the retromer complex and neurodegeneration, Mol Psychiatry, 24, 857, 10.1038/s41380-018-0221-3 · DOI · Paper page
- Chu, 2017, The retromer complex system in a transgenic mouse model of AD: Influence of age, Neurobiol Aging, 52, 32, 10.1016/j.neurobiolaging.2016.12.025 · DOI
- Li, 2020, Full recovery of the Alzheimer’s disease phenotype by gain of function of vacuolar protein sorting 35, Mol Psychiatry, 25, 2630, 10.1038/s41380-019-0364-x · DOI
- Vagnozzi, 2021, VPS35 regulates tau phosphorylation and neuropathology in tauopathy, Mol Psychiatry, 26, 6992, 10.1038/s41380-019-0453-x · DOI · Paper page
- Li, 2020, A pharmacological chaperone improves memory by reducing Aβ and tau neuropathology in a mouse model with plaques and tangles, Mol Neurodegener, 15, 1, 10.1186/s13024-019-0350-4 · DOI · Paper page
- Fronza, 2021, Effect of QTC-4-MeOBnE treatment on memory, neurodegeneration, and neurogenesis in a streptozotocin-induced mouse model of Alzheimer’s disease, ACS Chem Neurosci, 12, 109, 10.1021/acschemneuro.0c00615 · DOI
- Li, 2017, Genetic absence of ALOX5 protects from homocysteine-induced memory impairment, tau phosphorylation and synaptic pathology, Hum Mol Genet, 26, 1855, 10.1093/hmg/ddx088 · DOI
- Alzheimer’s Association, 2021, 2021 Alzheimer’s disease facts and figures, Alzheimers Dement, 17, 327, 10.1002/alz.12328 · DOI
- Hanley, 2020, Sorting nexins in protein homeostasis., Cells, 10, 17, 10.3390/cells10010017 · DOI
- Weeratunga, 2020, Recognizing the signals for endosomal trafficking, Curr Opin Cell Biol, 65, 17, 10.1016/j.ceb.2020.02.005 · DOI · Paper page
- Arbo, 2020, Endosomal dysfunction impacts extracellular vesicle release: Central role in Aβ pathology, Ageing Res Rev, 58, 101006, 10.1016/j.arr.2019.101006 · DOI
- Curtis, 2022, Association of retromer deficiency and tau pathology in Down syndrome, Ann Neurol, 91, 561, 10.1002/ana.26321 · DOI
- Curtis, 2020, Dysregulation of the retromer complex system in Down syndrome, Ann Neurol, 88, 137, 10.1002/ana.25752 · DOI · Paper page
- Martini, 2018, Past to future: What animal models have taught us about Alzheimer’s disease, J Alzheimers Dis, 64, S365, 10.3233/JAD-179917 · DOI
- Fu, 2019, A tau homeostasis signature is linked with the cellular and regional vulnerability of excitatory neurons to tau pathology, Neuron, 22, 47
- Paasila, 2022, Synapses, microglia, and lipids in Alzheimer’s disease, Front Neurosci, 15, 778822, 10.3389/fnins.2021.778822 · DOI
Cited by
Sorted by citations
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
- Li, J.-G., Blass, B. E., & Praticò, D.
- Affiliations
- Alzheimer’s Center at Temple, Lewis Katz School of Medicine, Philadelphia, PA, USA
- Venue
- Journal of Alzheimer's Disease
- Publisher
- SAGE Publications
- Published
- 2023-01-03
- Volume
- 91
- Issue
- 1
- Pages
- 463-469
- ISSN
- 1387-2877
- 1875-8908
- Cited by
- 4
- References
- 2
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
