Mitochondrial failure precedes amyloid beta plaques deposition in APP transgenic mice

2005 ◽  
Vol 38 (05) ◽  
Author(s):  
A Eckert ◽  
I Scherping ◽  
A Bonert ◽  
S Hauptmann ◽  
F Müller-Spahn ◽  
...  
Keyword(s):  
2018 ◽  
Vol 2 (2) ◽  
pp. 241-258 ◽  
Author(s):  
Shelli R. Kesler ◽  
Paul Acton ◽  
Vikram Rao ◽  
William J. Ray

Neurodegeneration in Alzheimer’s disease (AD) is associated with amyloid-beta peptide accumulation into insoluble amyloid plaques. The five-familial AD (5XFAD) transgenic mouse model exhibits accelerated amyloid-beta deposition, neuronal dysfunction, and cognitive impairment. We aimed to determine whether connectome properties of these mice parallel those observed in patients with AD. We obtained diffusion tensor imaging and resting-state functional magnetic resonance imaging data for four transgenic and four nontransgenic male mice. We constructed both structural and functional connectomes and measured their topological properties by applying graph theoretical analysis. We compared connectome properties between groups using both binarized and weighted networks. Transgenic mice showed higher characteristic path length in weighted structural connectomes and functional connectomes at minimum density. Normalized clustering and modularity were lower in transgenic mice across the upper densities of the structural connectome. Transgenic mice also showed lower small-worldness index in higher structural connectome densities and in weighted structural networks. Hyper-correlation of structural and functional connectivity was observed in transgenic mice compared with nontransgenic controls. These preliminary findings suggest that 5XFAD mouse connectomes may provide useful models for investigating the molecular mechanisms of AD pathogenesis and testing the effectiveness of potential treatments.


2020 ◽  
Vol 13 ◽  
Author(s):  
Sarah Houben ◽  
Marie-Ange de Fisenne ◽  
Kunie Ando ◽  
Virginie Vanden Dries ◽  
Luc Poncelet ◽  
...  

2009 ◽  
Vol 5 (4S_Part_17) ◽  
pp. e29-e29 ◽  
Author(s):  
Frank M. LaFerla ◽  
Hilda Martinez-Coria ◽  
Kim N. Green ◽  
Pradeep K. Banerjee

2008 ◽  
Vol 448 (2) ◽  
pp. 217-220 ◽  
Author(s):  
Marwan N. Sabbagh ◽  
Douglas G. Walker ◽  
Richard T. Reid ◽  
Tiffany Stadnick ◽  
Keshav Anand ◽  
...  

2006 ◽  
Vol 14 (7S_Part_12) ◽  
pp. P693-P694 ◽  
Author(s):  
Taro Bannai ◽  
Atsushi Iwata ◽  
Tatsuo Mano ◽  
Ryo Ohtomo ◽  
Gaku Ohtomo ◽  
...  

2019 ◽  
Vol 8 (1) ◽  
Author(s):  
Luís Costa-Marques ◽  
Katrin Arnold ◽  
Marie-Christine Pardon ◽  
Christiane Leovsky ◽  
Samantha Swarbrick ◽  
...  

Abstract Background We investigated early hallmarks of putative therapeutic effects following systemic transplantation of bone marrow derived macrophages (BM-M) in APP/PS1 transgenic mice. Method BM-M were transplanted into the tail vein and the animals analysed 1 month later. Results BM-M transplantation promoted the reduction of the amyloid beta [37-42] plaque number and size in the cortex and hippocampus of the treated mice, but no change in the more heavily modified pyroglutamate amyloid beta E3 plaques. The number of phenotypically ‘small’ microglia increased in the hippocampus. Astrocyte size decreased overall, indicating a reduction of activated astrocytes. Gene expression of interleukin 6 and 10, interferon-gamma, and prostaglandin E receptor 2 was significantly lower in the hippocampus, while interleukin 10 expression was elevated in the cortex of the treated mice. Conclusions BM-M systemically transplanted, promote a decrease in neuroinflammation and a limited reversion of amyloid pathology. This exploratory study may support the potential of BM-M or microglia-like cell therapy and further illuminates the mechanisms of action associated with such transplants.


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