scholarly journals Localization of gamma‐secretase subunit Aph‐1 in the central nervous system of Alzheimer's disease mouse model

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Guiqiong He ◽  
Shanquan Sun
2016 ◽  
Vol 60 (3) ◽  
pp. 305-315 ◽  
Author(s):  
Kathryn M. Munro ◽  
Amelia Nash ◽  
Martina Pigoni ◽  
Stefan F. Lichtenthaler ◽  
Jenny M. Gunnersen

Brain Repair ◽  
1990 ◽  
pp. 99-112
Author(s):  
Dan Lindholm ◽  
Christine Bandtlow ◽  
Matthias Spranger ◽  
Bastian Hengerer ◽  
Michael Meyer ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Peiqing Chen ◽  
Wenjuan Zhao ◽  
Yanjie Guo ◽  
Juan Xu ◽  
Ming Yin

CX3C chemokine ligand 1 (CX3CL1) is an intriguing chemokine belonging to the CX3C family. CX3CL1 is secreted by neurons and plays an important role in modulating glial activation in the central nervous system after binding to its sole receptor CX3CR1 which mainly is expressed on microglia. Emerging data highlights the beneficial potential of CX3CL1-CX3CR1 in the pathogenesis of Alzheimer’s disease (AD), a common progressive neurodegenerative disease, and in the progression of which neuroinflammation plays a vital role. Even so, the importance of CX3CL1/CX3CR1 in AD is still controversial and needs further clarification. In this review, we make an attempt to present a concise map of CX3CL1-CX3CR1 associated with AD to find biomarkers for early diagnosis or therapeutic interventions.


2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Koji Hori ◽  
Kimiko Konishi ◽  
Masayuki Tani ◽  
Hiroi Tomioka ◽  
Ryo Akita ◽  
...  

We review the utility of serum anticholinergic activity (SAA) as a peripheral marker of anticholinergic activity (AA) in the central nervous system (CAA). We hypothesize that the compensatory mechanisms of the cholinergic system do not contribute to SAA if their system is intact and that if central cholinergic system deteriorates alone in conditions such as Alzheimer’s disease or Lewy body dementia, CAA and SAA are caused by way of hyperactivity of inflammatory system and SAA is a marker of the anticholinergic burden in CNS. Taking into account the diurnal variations in the plasma levels of corticosteroids, which are thought to affect SAA, it should be measured at noon or just afterward.


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