scholarly journals Peripheral Mechanosensory Neuron Dysfunction Underlies Tactile and Behavioral Deficits in Mouse Models of ASDs

Cell ◽  
2016 ◽  
Vol 166 (2) ◽  
pp. 299-313 ◽  
Author(s):  
Lauren L. Orefice ◽  
Amanda L. Zimmerman ◽  
Anda M. Chirila ◽  
Steven J. Sleboda ◽  
Joshua P. Head ◽  
...  
Keyword(s):  
Mouse Models ◽  
Behavioral Deficits ◽  
Mechanosensory Neuron

scholarly journals Intranasal oxytocin administration ameliorates social behavioral deficits in a POGZWT/Q1038R mouse model of autism spectrum disorder

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Kohei Kitagawa ◽  
Kensuke Matsumura ◽  
Masayuki Baba ◽  
Momoka Kondo ◽  
Tomoya Takemoto ◽  
...  
Keyword(s):  
Autism Spectrum Disorder ◽  
Social Behavior ◽  
Mouse Model ◽  
Mouse Models ◽  
De Novo ◽  
Neurodevelopmental Disorder ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
De Novo Mutation ◽  
Behavioral Deficits

AbstractAutism spectrum disorder (ASD) is a highly prevalent neurodevelopmental disorder characterized by core symptoms of impaired social behavior and communication. Recent studies have suggested that the oxytocin system, which regulates social behavior in mammals, is potentially involved in ASD. Mouse models of ASD provide a useful system for understanding the associations between an impaired oxytocin system and social behavior deficits. However, limited studies have shown the involvement of the oxytocin system in the behavioral phenotypes in mouse models of ASD. We have previously demonstrated that a mouse model that carries the ASD patient-derived de novo mutation in the pogo transposable element derived with zinc finger domain (POGZWT/Q1038R mice), showed ASD-like social behavioral deficits. Here, we have explored whether oxytocin (OXT) administration improves impaired social behavior in POGZWT/Q1038R mice and found that intranasal oxytocin administration effectively restored the impaired social behavior in POGZWT/Q1038R mice. We also found that the expression level of the oxytocin receptor gene (OXTR) was low in POGZWT/Q1038R mice. However, we did not detect significant changes in the number of OXT-expressing neurons between the paraventricular nucleus of POGZWT/Q1038R mice and that of WT mice. A chromatin immunoprecipitation assay revealed that POGZ binds to the promoter region of OXTR and is involved in the transcriptional regulation of OXTR. In summary, our study demonstrate that the pathogenic mutation in the POGZ, a high-confidence ASD gene, impairs the oxytocin system and social behavior in mice, providing insights into the development of oxytocin-based therapeutics for ASD.

Dihydromyricetin Ameliorates Behavioral Deficits and Reverses Neuropathology of Transgenic Mouse Models of Alzheimer’s Disease

2014 ◽  
Vol 39 (6) ◽  
pp. 1171-1181 ◽  
Author(s):  
Jing Liang ◽  
A. Kerstin Lindemeyer ◽  
Yi Shen ◽  
Héctor E. López-Valdés ◽  
Hilda Martínez-Coria ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Transgenic Mouse ◽  
Mouse Models ◽  
Transgenic Mouse Models ◽  
Behavioral Deficits

scholarly journals Neuron Loss in Transgenic Mouse Models of Alzheimer's Disease

2010 ◽  
Vol 2010 ◽  
pp. 1-6 ◽  
Author(s):  
Oliver Wirths ◽  
Thomas A. Bayer
Keyword(s):  
Transgenic Mouse ◽  
Mouse Models ◽  
Amyloid Plaque ◽  
Model Systems ◽  
Transgenic Mouse Models ◽  
Behavioral Deficits ◽  
Neuron Loss ◽  
Plaque Pathology ◽  
Initial Generation ◽  
Alzheimers’S Disease

Since their initial generation in the mid 1990s, transgenic mouse models of Alzheimers's disease (AD) have been proven to be valuable model systems which are indispensable for modern AD research. Whereas most of these models are characterized by extensive amyloid plaque pathology, inflammatory changes and often behavioral deficits, modeling of neuron loss was much less successful. The present paper discusses the current achievements of modeling neuron loss in transgenic mouse models based on APP/Aβand Tau overexpression and provides an overview of currently available AD mouse models showing these pathological alterations.

scholarly journals Long-term caffeine treatment of Alzheimer mouse models ameliorates behavioural deficits and neuron loss and promotes cellular and molecular markers of neurogenesis

2021 ◽  
Author(s):  
Martina Stazi ◽  
Sandra Lehmann ◽  
M. Sadman Sakib ◽  
Tonatiuh Pena-Centeno ◽  
Luca Büschgens ◽  
...  
Keyword(s):  
Mouse Models ◽  
Hippocampal Neuron ◽  
Amyloid Β ◽  
Synaptic Function ◽  
Sequencing Analysis ◽  
Behavioral Deficits ◽  
Altered Expression ◽  
Neuron Loss ◽  
App Processing

AbstractEpidemiological studies indicate that the consumption of caffeine, the most commonly ingested psychoactive substance found in coffee, tea or soft drinks, reduces the risk of developing Alzheimer’s disease (AD). Previous treatment studies with transgenic AD mouse models reported a reduced amyloid plaque load and an amelioration of behavioral deficits. It has been further shown that moderate doses of caffeine have the potential to attenuate the health burden in preclinical mouse models of a variety of brain disorders (reviewed in Cunha in J Neurochem 139:1019–1055, 2016). In the current study, we assessed whether long-term caffeine consumption affected hippocampal neuron loss and associated behavioral deficits in the Tg4-42 mouse model of AD. Treatment over a 4-month period reduced hippocampal neuron loss, rescued learning and memory deficits, and ameliorated impaired neurogenesis. Neuron-specific RNA sequencing analysis in the hippocampus revealed an altered expression profile distinguished by the up-regulation of genes linked to synaptic function and processes, and to neural progenitor proliferation. Treatment of 5xFAD mice, which develop prominent amyloid pathology, with the same paradigm also rescued behavioral deficits but did not affect extracellular amyloid-β (Aβ) levels or amyloid precursor protein (APP) processing. These findings challenge previous assumptions that caffeine is anti-amyloidogenic and indicate that the promotion of neurogenesis might play a role in its beneficial effects.

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