pubs.bib

@article{fowlerExtracellularVesiclesDerived2020,
  title = {Extracellular Vesicles Derived from Postmortem Human Brain Tissue Contain Seed-competent {{C}}-terminal Tau Fragments, and Provide Proteomic Clues to the Identity of Selectively Vulnerable Cell Populations in Human Tauopathies: {{Molecular}} and Cell Biology: {{Tau}}-related Mechanisms},
  shorttitle = {Extracellular Vesicles Derived from Postmortem Human Brain Tissue Contain Seed-competent {{C}}-terminal Tau Fragments, and Provide Proteomic Clues to the Identity of Selectively Vulnerable Cell Populations in Human Tauopathies},
  author = {Fowler, Stephanie L. and Bez, Sumi and Gaur, Pallavi and Miller, Chelsea and Turkes, Emir and Schaler, Ari and Hernandez Villegas, Nancy E. and Perez-Gonzalez, Rocio and Levy, Efrat and Duff, Karen E.},
  year = {2020},
  month = dec,
  volume = {16},
  issn = {1552-5260, 1552-5279},
  doi = {10.1002/alz.042870},
  abstract = {Background: Pathological tau is spread along anatomically connected networks, originating in areas containing particularly vulnerable cell populations. It is hypothesized that tau is released and spread as free tau, or via extracellular vesicles (EVs) that include exosomes (30-150 nm), microvesicles (100-1000 nm), and apoptotic bodies (1000-5000 nM). While a variety of different EV tau species have been identified in tissue, cells, and bio-fluids, EV tau has not yet been described from human post-mortem tauopathy brain tissue.},
  copyright = {All rights reserved},
  file = {/home/eturkes/Documents/reference/zotero/fowler-2020-extracellular_vesicles_derived_from_postmortem.pdf},
  journal = {Alzheimer's \& Dementia},
  language = {en},
  number = {S2}
}

@article{kirykIntelliCageToolMeasuring2020,
  title = {{{IntelliCage}} as a Tool for Measuring Mouse Behavior \textendash{} 20 Years Perspective},
  author = {Kiryk, Anna and Janusz, Artur and Zglinicki, Bartosz and Turkes, Emir and Knapska, Ewelina and Konopka, Witold and Lipp, Hans-Peter and Kaczmarek, Leszek},
  year = {2020},
  month = jun,
  volume = {388},
  pages = {112620},
  issn = {01664328},
  doi = {10.1016/j.bbr.2020.112620},
  abstract = {Since the 1980s, we have witnessed the rapid development of genetically modified mouse models of human diseases. A large number of transgenic and knockout mice have been utilized in basic and applied research, including models of neurodegenerative and neuropsychiatric disorders. To assess the biological function of mutated genes, modern techniques are critical to detect changes in behavioral phenotypes. We review the IntelliCage, a high-throughput system that is used for behavioral screening and detailed analyses of complex behaviors in mice. The IntelliCage was introduced almost two decades ago and has been used in over 150 studies to assess both spontaneous and cognitive behaviors. We present a critical analysis of experimental data that have been generated using this device.},
  copyright = {All rights reserved},
  file = {/home/eturkes/Documents/reference/zotero/kiryk-2020-intellicage_as_a_tool_for_measuring_mouse.pdf},
  journal = {Behavioural Brain Research},
  language = {en}
}

@article{turkesCellTypeSpecific2020,
  title = {Cell-type Specific Selective Vulnerability to Pathological Tau in {{Alzheimer}}'s Disease: {{Molecular}} and Cell Biology/Tau},
  shorttitle = {Cell-type Specific Selective Vulnerability to Pathological Tau in {{Alzheimer}}'s Disease},
  author = {Turkes, Emir and Duff, Karen E.},
  year = {2020},
  month = dec,
  volume = {16},
  issn = {1552-5260, 1552-5279},
  doi = {10.1002/alz.043149},
  abstract = {Background: Region-specific neuronal subpopulations known to be selectively vulnerable to Tau pathology, as characterized in our previous work (Fu et al., 2019), were identified across several public single-nucleus RNA sequencing datasets from non-diseased human in order to derive putative properties and mechanisms that drive vulnerability. Methods: We analyzed datasets from the Allen Brain Institute (Hodge et al., 2019), Broad Institute (Habib et al., 2017), and Polo group (Grubman et al., 2019). After QC, dimensionality reduction, and clustering, vulnerable and invulnerable neuronal subpopulations were identified using anatomical metadata and marker genes. Differential expression between subpopulations were performed using the Wilcoxon test, while differential pathway analysis was carried out using the GSVA algorithm. Result: We were able to identify putative subpopulations across a range of presumed vulnerability as defined by classical pathological staging. Several themes emerge from differential pathway analysis of these subpopulations in various comparisons, including those related to vesicle-mediated exocytosis activity and synaptic plasticity. Following further drilling down of these pathways for their association with vulnerability, pathways will be systematically screened in a model system measuring Tau aggregation. Conclusion: Extensive pathway analysis of neuronal subpopulations selectively vulnerable to Tau pathology in human single-nucleus RNA sequencing data reveal significant heterogeneity between neurons that may be responsible for driving pathological status.},
  copyright = {All rights reserved},
  file = {/home/eturkes/Documents/reference/zotero/turkes-2020-cell‐type_specific_selective_vulnerability_to.pdf},
  journal = {Alzheimer's \& Dementia},
  language = {en},
  number = {S3}
}