| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Brent Race, Katie Williams, James F Striebel, Bruce Chesebr. Prion-associated cerebral amyloid angiopathy is not exacerbated by human phosphorylated tau aggregates in scrapie-infected mice expressing anchorless prion protein. Neurobiology of disease. vol 144. 2021-09-24. PMID:32829029. |
these mice expressed human tau but lacked both mouse tau and gpi-anchored prp. |
2021-09-24 |
2023-08-13 |
mouse |
| Brent Race, Katie Williams, James F Striebel, Bruce Chesebr. Prion-associated cerebral amyloid angiopathy is not exacerbated by human phosphorylated tau aggregates in scrapie-infected mice expressing anchorless prion protein. Neurobiology of disease. vol 144. 2021-09-24. PMID:32829029. |
nevertheless, the accumulation of aggregated, phosphorylated human tau and its association with prp amyloid plaques failed to alter the timing or course of the clinical disease observed. |
2021-09-24 |
2023-08-13 |
mouse |
| Brent Race, Katie Williams, James F Striebel, Bruce Chesebr. Prion-associated cerebral amyloid angiopathy is not exacerbated by human phosphorylated tau aggregates in scrapie-infected mice expressing anchorless prion protein. Neurobiology of disease. vol 144. 2021-09-24. PMID:32829029. |
these data suggest that human tau does not contribute to the pathogenesis of mouse prp amyloid brain disease and raise the possibility that tau may also not be pathogenic in human prp amyloid disease. |
2021-09-24 |
2023-08-13 |
mouse |
| b' Kate\\xc5\\x99ina Men\\xc5\\xa1\\xc3\\xadkov\\xc3\\xa1, Radoslav Mat\\xc4\\x9bj, Eva Parobkov\\xc3\\xa1, Magdalena Sm\\xc4\\x9bt\\xc3\\xa1kov\\xc3\\xa1, Petr Ka\\xc5\\x88ovsk\\xc3\\xb. PART and ARTAG tauopathies at a relatively young age as a concomitant finding in sporadic Creutzfeldt-Jakob disease. Prion. vol 15. issue 1. 2021-09-24. PMID:34224311.' |
interactions between prion protein (prp) and tau protein have long been discussed, especially in relation to the pathogenesis of neurodegenerative diseases. |
2021-09-24 |
2023-08-13 |
Not clear |
| b' Kate\\xc5\\x99ina Men\\xc5\\xa1\\xc3\\xadkov\\xc3\\xa1, Radoslav Mat\\xc4\\x9bj, Eva Parobkov\\xc3\\xa1, Magdalena Sm\\xc4\\x9bt\\xc3\\xa1kov\\xc3\\xa1, Petr Ka\\xc5\\x88ovsk\\xc3\\xb. PART and ARTAG tauopathies at a relatively young age as a concomitant finding in sporadic Creutzfeldt-Jakob disease. Prion. vol 15. issue 1. 2021-09-24. PMID:34224311.' |
molecular interactions between prp and tau protein have been demonstrated in animal models; the role is attributed to the structural properties of misfolded isoform of the host-encoded prion protein (prp |
2021-09-24 |
2023-08-13 |
Not clear |
| Matteo Manca, Allison Krau. Defining the Protein Seeds of Neurodegeneration using Real-Time Quaking-Induced Conversion Assays. Biomolecules. vol 10. issue 9. 2021-09-07. PMID:32854212. |
in this review we discuss the application of rt-quic assays as diagnostic, experimental, and structural tools for detection and discrimination of prp prions, tau, and αsyn protein seeds. |
2021-09-07 |
2023-08-13 |
human |
| Grace I Hallinan, Md Rejaul Hoq, Manali Ghosh, Frank S Vago, Anllely Fernandez, Holly J Garringer, Ruben Vidal, Wen Jiang, Bernardino Ghett. Structure of Tau filaments in Prion protein amyloidoses. Acta neuropathologica. vol 142. issue 2. 2021-08-16. PMID:34128081. |
here, we analyze tau filaments isolated from the brain of individuals affected by prion-protein cerebral amyloid angiopathy (prp-caa) with a nonsense mutation in the prnp gene that leads to early termination of translation of prp (q160ter or q160x), and gerstmann-sträussler-scheinker (gss) disease, with a missense mutation in the prnp gene that leads to an amino acid substitution at residue 198 (f198s) of prp. |
2021-08-16 |
2023-08-13 |
human |
| Victor V Dyakin, Thomas M Wisniewski, Abel Lajth. Racemization in Post-Translational Modifications Relevance to Protein Aging, Aggregation and Neurodegeneration: Tip of the Iceberg. Symmetry. vol 13. issue 3. 2021-08-06. PMID:34350031. |
the brain region, cell type, and age-dependent racemization critically influence the functions of many intracellular, membrane-bound, and extracellular proteins including amyloid precursor protein (app), tau, prp, huntingtin, α-synuclein, myelin basic protein (mbp), and collagen. |
2021-08-06 |
2023-08-13 |
Not clear |
| Laia Lidón, Laura Llaó-Hierro, Mario Nuvolone, Adriano Aguzzi, Jesús Ávila, Isidro Ferrer, José Antonio Del Río, Rosalina Gaví. Tau Exon 10 Inclusion by PrP International journal of molecular sciences. vol 22. issue 10. 2021-06-17. PMID:34065232. |
tau exon 10 inclusion by prp tau protein is largely responsible for tauopathies, including alzheimer's disease (ad), where it accumulates in the brain as insoluble aggregates. |
2021-06-17 |
2023-08-13 |
Not clear |
| Laia Lidón, Laura Llaó-Hierro, Mario Nuvolone, Adriano Aguzzi, Jesús Ávila, Isidro Ferrer, José Antonio Del Río, Rosalina Gaví. Tau Exon 10 Inclusion by PrP International journal of molecular sciences. vol 22. issue 10. 2021-06-17. PMID:34065232. |
in this sense, one of the several factors that regulate alternative splicing of tau is gsk3β, whose activity is inhibited by the cellular prion protein (prp |
2021-06-17 |
2023-08-13 |
Not clear |
| George A Carlson, Stanley B Prusine. How an Infection of Sheep Revealed Prion Mechanisms in Alzheimer's Disease and Other Neurodegenerative Disorders. International journal of molecular sciences. vol 22. issue 9. 2021-06-15. PMID:34064393. |
we compare diseases caused by misfolding and aggregation of app-derived aβ peptides, tau, and α-synuclein with prp prion disorders and argue for the classification of nds caused by misfolding of these proteins as prion diseases. |
2021-06-15 |
2023-08-13 |
Not clear |
| Grant T Corbett, Zemin Wang, Wei Hong, Marti Colom-Cadena, Jamie Rose, Meichen Liao, Adhana Asfaw, Tia C Hall, Lai Ding, Alexandra DeSousa, Matthew P Frosch, John Collinge, David A Harris, Michael S Perkinton, Tara L Spires-Jones, Tracy L Young-Pearse, Andrew Billinton, Dominic M Wals. PrP is a central player in toxicity mediated by soluble aggregates of neurodegeneration-causing proteins. Acta neuropathologica. vol 139. issue 3. 2021-05-17. PMID:31853635. |
here, we show that soluble aggregates of α-synuclein and tau bind to plate-immobilized prp in vitro and on mouse cortical neurons, and that this binding requires at least one of the same n-terminal sites at which soluble aβ aggregates bind. |
2021-05-17 |
2023-08-13 |
mouse |
| Grant T Corbett, Zemin Wang, Wei Hong, Marti Colom-Cadena, Jamie Rose, Meichen Liao, Adhana Asfaw, Tia C Hall, Lai Ding, Alexandra DeSousa, Matthew P Frosch, John Collinge, David A Harris, Michael S Perkinton, Tara L Spires-Jones, Tracy L Young-Pearse, Andrew Billinton, Dominic M Wals. PrP is a central player in toxicity mediated by soluble aggregates of neurodegeneration-causing proteins. Acta neuropathologica. vol 139. issue 3. 2021-05-17. PMID:31853635. |
moreover, soluble aggregates of tau, α-synuclein and aβ cause both functional (impairment of ltp) and structural (neuritic dystrophy) compromise and these deficits are absent when prp is ablated, knocked-down, or when neurons are pre-treated with anti-prp blocking antibodies. |
2021-05-17 |
2023-08-13 |
mouse |
| Grant T Corbett, Zemin Wang, Wei Hong, Marti Colom-Cadena, Jamie Rose, Meichen Liao, Adhana Asfaw, Tia C Hall, Lai Ding, Alexandra DeSousa, Matthew P Frosch, John Collinge, David A Harris, Michael S Perkinton, Tara L Spires-Jones, Tracy L Young-Pearse, Andrew Billinton, Dominic M Wals. PrP is a central player in toxicity mediated by soluble aggregates of neurodegeneration-causing proteins. Acta neuropathologica. vol 139. issue 3. 2021-05-17. PMID:31853635. |
using an all-human experimental paradigm involving: (1) isogenic ipsc-derived neurons expressing or lacking prnp, and (2) aqueous extracts from brains of individuals who died with alzheimer's disease, dementia with lewy bodies, and pick's disease, we demonstrate that aβ, α-synuclein and tau are toxic to neurons in a manner that requires prp |
2021-05-17 |
2023-08-13 |
mouse |
| Shaopei Li, Kagan Kerma. Electrochemical biosensors for biometal-protein interactions in neurodegenerative diseases. Biosensors & bioelectronics. vol 179. 2021-05-14. PMID:33578115. |
the focus will be drawn on disease-causing biomarkers such as amyloid-β (aβ) and tau proteins for ad, α-synuclein (α-syn) for pd, and prion proteins (prp). |
2021-05-14 |
2023-08-13 |
Not clear |
| Antonio Monaco, Veronica Maffia, Nicolina Cristina Sorrentino, Irene Sambri, Yulia Ezhova, Teresa Giuliano, Vincenzo Cacace, Edoardo Nusco, Maria De Risi, Elvira De Leonibus, Thomas Schrader, Frank-Gerrit Klärner, Gal Bitan, Alessandro Frald. The Amyloid Inhibitor CLR01 Relieves Autophagy and Ameliorates Neuropathology in a Severe Lysosomal Storage Disease. Molecular therapy : the journal of the American Society of Gene Therapy. vol 28. issue 4. 2021-04-06. PMID:32087148. |
by studying a mouse model of mucopolysaccharidosis (mps) type iiia, one of the most common and severe forms of lsds, we found that multiple amyloid proteins including α-synuclein, prion protein (prp), tau, and amyloid β progressively aggregate in the brain. |
2021-04-06 |
2023-08-13 |
mouse |
| Yan-Ling Zhou, Shu-Qing Liu, Bin Yuan, Ning L. The expression of insulin-like growth factor-1 in senior patients with diabetes and dementia. Experimental and therapeutic medicine. vol 13. issue 1. 2020-10-01. PMID:28123476. |
the levels of igf-1, aβ, tau protein positive rate, prp, foxo protein, p-pi3k, and p-akt in group a were significantly higher than that in group b, which was higher than in groups c and d. the results between groups a and b, but not groups c and d, were statistically significant (p<0.05). |
2020-10-01 |
2023-08-13 |
Not clear |
| Yan-Ling Zhou, Shu-Qing Liu, Bin Yuan, Ning L. The expression of insulin-like growth factor-1 in senior patients with diabetes and dementia. Experimental and therapeutic medicine. vol 13. issue 1. 2020-10-01. PMID:28123476. |
thus, igf-1 can adjust the expression of prp and foxo through p-pi3k/akt pathway and further impact the formation of aβ and tau protein, leading to dementia. |
2020-10-01 |
2023-08-13 |
Not clear |
| Michael A Metrick, Natalia do Carmo Ferreira, Eri Saijo, Andrew G Hughson, Allison Kraus, Christina Orrú, Michael W Miller, Gianluigi Zanusso, Bernardino Ghetti, Michele Vendruscolo, Byron Caughe. Million-fold sensitivity enhancement in proteopathic seed amplification assays for biospecimens by Hofmeister ion comparisons. Proceedings of the National Academy of Sciences of the United States of America. vol 116. issue 46. 2020-04-06. PMID:31641070. |
here, we systematically investigated the effects of the ionic environment on the polymerization of tau, α-synuclein, and the prion protein (prp) induced by aggregates in biospecimens. |
2020-04-06 |
2023-08-13 |
Not clear |
| Guilherme A P de Oliveira, Yraima Cordeiro, Jerson L Silva, Tuane C R G Vieir. Liquid-liquid phase transitions and amyloid aggregation in proteins related to cancer and neurodegenerative diseases. Advances in protein chemistry and structural biology. vol 118. 2020-04-02. PMID:31928729. |
amyloid formation would correspond to an irreversible liquid-to-solid transition, as clearly observed in the case of prp, tdp43, fus/tls and tau protein in neurodegenerative pathologies as well as with the mutant tumor suppressor p53 in cancer. |
2020-04-02 |
2023-08-13 |
Not clear |