scholarly journals Identifying early markers of synaptic dysfunction in a mouse model of tauopathy

2020 ◽  
Vol 16 (S3) ◽  
Author(s):  
Soraya Meftah ◽  
Jonathan Witton ◽  
Annalisa Cavallini ◽  
Tracey K. Murray ◽  
Lukasz Jankowski ◽  
...  
Keyword(s):  
Mouse Model ◽  
Synaptic Dysfunction ◽  
Early Markers

scholarly journals Imbalance in the response of pre- and post-synaptic components to amyloidopathy

2019 ◽  
Author(s):  
Terri-Leigh Stephen ◽  
Francesco Tamagnini ◽  
Judith Piegsa ◽  
Katherine Sung ◽  
Joshua Harvey ◽  
...  
Keyword(s):  
Mouse Model ◽  
Synaptic Dysfunction ◽  
Functional Impairments ◽  
Synaptic Terminals ◽  
Diffuse Part ◽  
Initial Area ◽  
Synapse Density ◽  
Synaptic Dynamics ◽  
Underlying Pathology ◽  
Over Time

AbstractAlzheimer’s disease (AD)-associated synaptic dysfunction drives the progression of pathology from its earliest stages. Aβ species, both soluble and in plaque deposits, have been causally related to the progressive, structural and functional impairments observed in AD. It is, however, still unclear how Aβ plaques develop over time and how they progressively affect local synapse density and turnover. Here we observed, in a mouse model of AD, that Aβ plaques grow faster in the earlier stages of the disease and if their initial area is > 500 µm2; this may be due to deposition occurring in the diffuse part of the plaque. In addition, synaptic turnover is higher in the presence of amyloid pathology and this is paralleled by a reduction in pre-but not post-synaptic densities. Plaque proximity does not appear to have an impact on synaptic dynamics. These observations indicate an imbalance in the response of the pre- and post-synaptic terminals and that therapeutics, alongside targeting the underlying pathology, need to address changes in synapse dynamics.

scholarly journals Impaired AMPA signaling and cytoskeletal alterations induce early synaptic dysfunction in a mouse model of Alzheimer's disease

Aging Cell ◽  
2018 ◽  
Vol 17 (4) ◽  
pp. e12791 ◽  
Author(s):  
David Baglietto-Vargas ◽  
Gilberto Aleph Prieto ◽  
Agenor Limon ◽  
Stefania Forner ◽  
Carlos J. Rodriguez-Ortiz ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Synaptic Dysfunction ◽  
Model Of Alzheimer’S Disease

scholarly journals Deficits in hippocampal-dependent transfer generalization learning accompany synaptic dysfunction in a mouse model of amyloidosis

Hippocampus ◽  
2015 ◽  
Vol 26 (4) ◽  
pp. 455-471 ◽  
Author(s):  
Karienn S. Montgomery ◽  
George Edwards ◽  
Yona Levites ◽  
Ashok Kumar ◽  
Catherine E. Myers ◽  
...  
Keyword(s):  
Mouse Model ◽  
Synaptic Dysfunction

scholarly journals Food Allergy Adjuvant and Early Immune Effects of Oral Exposure to Known and Suspected Gut Barrier Disruptors 

2020 ◽  
Author(s):  
Elena Drønen ◽  
Unni Nygaard ◽  
Ellen Namork ◽  
Hubert Dirven
Keyword(s):  
Food Allergy ◽  
Mouse Model ◽  
Peanut Allergy ◽  
Intestinal Barrier ◽  
Oral Exposure ◽  
Gut Barrier ◽  
Interleukin 33 ◽  
Early Markers ◽  
Peanut Extract ◽  
Early Effects

Abstract Background: Exposure to adjuvants with a food allergen has been shown to promote sensitization and development of food allergy in animal models. Barrier disrupting capacities have been suggested to be one mechanism of adjuvant action. In this study, we investigated how gut barrier disrupting compounds affected food allergy development in a mouse model of peanut allergy. Sensitization and clinical peanut allergy in C3H/HEOuJ mice were assessed after repeated oral exposure to peanut extract together with cholera toxin (CT), the mycotoxin deoxynivalenol (DON), house dust mite (HDM) or the pesticide glyphosate (GLY). In addition, we investigated early effects 4 to 48 hours after a single exposure to the compounds, by assessing markers of intestinal barrier permeability, alarmin production, intestinal epithelial responses, and local immune responses.Results: CT and DON exerted adjuvant effects on peanut allergy development assessed as clinical anaphylaxis in mice. The early markers were consistently only affected by DON, observed as increased IL-33 (interleukin 33) and thymic stromal lymphopoietin (TSLP) alarmin production in intestines and Interleukin 33 receptor ST2 in serum. DON also induced an inflammatory immune response in lymph node cells stimulated with lipopolysaccharide (LPS). HDM and GLY did not promote clinical food allergy and affected few (or none) of the early markers at the present doses.Conclusions: Oral exposure to CT and DON promoted development of clinical anaphylaxis in the peanut allergy mouse model. DON, but not CT, affected the early markers measured in the present study, indicating that DON and CT have different modes of action at the early stages of peanut sensitization.

P4-052: Dissociation of synaptic dysfunction and behavior in a tauopathy mouse model (PrP-MAPT) of Alzheimer's disease

2009 ◽  
Vol 5 (4S_Part_15) ◽  
pp. P446-P447
Author(s):  
Margaret Zaleska ◽  
Robert A. Crozier ◽  
Nathalie Breysse ◽  
Reka Hosszu ◽  
Mark R. Bowlby ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Synaptic Dysfunction ◽  
And Behavior

Corrigendum to “Anxiety, neuroinflammation, cholinergic and GABAergic abnormalities are early markers of Gulf War illness in a mouse model of the disease” [Brain Res. 1681 (2018) 34–43]

2018 ◽  
Vol 1688 ◽  
pp. 113-115
Author(s):  
Isabel Carreras ◽  
Nurgul Aytan ◽  
Tiffany Mellott ◽  
Ji-Kyung Choi ◽  
Margaret Lehar ◽  
...  
Keyword(s):  
Mouse Model ◽  
Gulf War ◽  
Gulf War Illness ◽  
Early Markers
Sign in / Sign up

Export Citation Format

Share Document