Lomoio, Selene <br/><br/>
Beta-amyloid overload does not directly correlate with SAPK/JNK activation and tau protein phosphorylation in the cerebellar cortex of Ts65Dn mice.  [electronic resource] 

 -  Brain research  Nov 2009 
 - 198-206 p.  digital 
<br/><br/> Publication Type: Journal Article 
<br/><br/><label>ISSN: </label>1872-6240 
<br/><br/><label>Standard No.: </label>10.1016/j.brainres.2009.08.052  doi 
<br/><br/><label>Subjects--Topical Terms: </label><br/>Amyloid beta-Peptides--genetics<br/>Animals<br/>Axons--metabolism<br/>Cerebellum--metabolism<br/>Disease Models, Animal<br/>Down Syndrome--genetics<br/>Female<br/>Genetic Predisposition to Disease--genetics<br/>Interneurons--metabolism<br/>JNK Mitogen-Activated Protein Kinases--metabolism<br/>Male<br/>Mice<br/>Mice, Transgenic<br/>Mitogen-Activated Protein Kinase 8--metabolism<br/>Nerve Degeneration--genetics<br/>Neuroglia--metabolism<br/>Phosphorylation<br/>Purkinje Cells--metabolism<br/>Signal Transduction--physiology<br/>Tauopathies--genetics<br/>Trisomy--genetics<br/>tau Proteins--metabolism