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

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.

2004 ◽  
Vol 25 ◽  
pp. S11
Author(s):  
Thomas A. Bayer ◽  
Oliver Wirths ◽  
Caty Casas ◽  
Patrick Benoit ◽  
Christoph Schmitz ◽  
...  

2014 ◽  
Vol 39 (6) ◽  
pp. 1171-1181 ◽  
Author(s):  
Jing Liang ◽  
A. Kerstin Lindemeyer ◽  
Yi Shen ◽  
Héctor E. López-Valdés ◽  
Hilda Martínez-Coria ◽  
...  

2013 ◽  
pp. 177-190
Author(s):  
Kebreten F. Manaye ◽  
Peter R. Mouton

2020 ◽  
Vol 21 (21) ◽  
pp. 8144
Author(s):  
Oliver Wirths ◽  
Silvia Zampar

Transgenic mouse models represent an essential tool for the exploration of Alzheimer’s disease (AD) pathological mechanisms and the development of novel treatments, which at present provide only symptomatic and transient effects. While a variety of mouse models successfully reflects the main neuropathological hallmarks of AD, such as extracellular amyloid-β (Aβ) deposits, intracellular accumulation of Tau protein, the development of micro- and astrogliosis, as well as behavioral deficits, substantial neuron loss, as a key feature of the disease, seems to be more difficult to achieve. In this review, we summarize information on classic and more recent transgenic mouse models for AD, focusing in particular on loss of pyramidal, inter-, and cholinergic neurons. Although the cause of neuron loss in AD is still a matter of scientific debate, it seems to be linked to intraneuronal Aβ accumulation in several transgenic mouse models, especially in pyramidal neurons.


2005 ◽  
Vol 19 (3) ◽  
pp. 229-235 ◽  
Author(s):  
Andrew P. Lane ◽  
Haiqing Zhao ◽  
Randall R. Reed

Background Olfactory loss is a significant health problem that remains incompletely understood. The development of suitable animal models is essential to the progress of human olfactory loss research. Recent advancements in transgenic technology allow the creation of model systems to address causes of olfactory neuron dysfunction. Methods This review describes two transgenic mouse models with potential usefulness in the study of olfactory loss and highlights the molecular techniques that underlie the development of such systems. Results Genetic constructs generated using standard molecular biological techniques are introduced into mouse germ lines either by homologous recombination or by random integration. One construct (UbI7) places the olfactory receptor I7 under control of the olfactory marker protein promoter. The other two constructs (TI) act together to direct expression of cytokines in the olfactory epithelium, creating a novel approach to the study of inflammatory olfactory loss. Conclusions Powerful scientific tools now exist to develop animal models useful to the study of human olfactory disease. Transgenic olfactory neurons from the UbI7 mouse strain will respond to known odorants, facilitating experiments that examine in vitro modulation of olfactory neuron function. The ability to express specific genes in the olfactory mucosa of the TI mouse has great potential in elucidating the role of cytokines in the development of olfactory dysfunction in vivo.


2014 ◽  
Vol 39 (7) ◽  
pp. 1403-1403 ◽  
Author(s):  
Jing Liang ◽  
Héctor E. López-Valdés ◽  
Hilda Martínez-Coria ◽  
A. Kerstin Lindemeyer ◽  
Yi Shen ◽  
...  

Diabetes ◽  
1990 ◽  
Vol 39 (8) ◽  
pp. 879-884 ◽  
Author(s):  
M. A. Lipes ◽  
G. S. Eisenbarth

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