Title |
Pro-inflammatory interleukin-18 increases Alzheimer’s disease-associated amyloid-β production in human neuron-like cells
|
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Published in |
Journal of Neuroinflammation, August 2012
|
DOI | 10.1186/1742-2094-9-199 |
Pubmed ID | |
Authors |
Elina M Sutinen, Tuula Pirttilä, George Anderson, Antero Salminen, Johanna O Ojala |
Abstract |
Alzheimer's disease (AD) involves increased accumulation of amyloid-β (Aβ) plaques and neurofibrillary tangles as well as neuronal loss in various regions of the neocortex. Neuroinflammation is also present, but its role in AD is not fully understood. We previously showed increased levels of pro-inflammatory cytokine interleukin-18 (IL-18) in different regions of AD brains, where it co-localized with Aβ-plaques, as well as the ability of IL-18 to increase expression of glycogen synthase kinase-3β (GSK-3β) and cyclin dependent kinase 5, involved in hyperphosphorylation of tau-protein. Elevated IL-18 has been detected in several risk conditions for AD, including obesity, type-II diabetes, and cardiovascular diseases as well as in stress. |
X Demographics
Geographical breakdown
Country | Count | As % |
---|---|---|
Mexico | 1 | 50% |
Spain | 1 | 50% |
Demographic breakdown
Type | Count | As % |
---|---|---|
Members of the public | 2 | 100% |
Mendeley readers
Geographical breakdown
Country | Count | As % |
---|---|---|
Germany | 1 | <1% |
Unknown | 166 | 99% |
Demographic breakdown
Readers by professional status | Count | As % |
---|---|---|
Researcher | 34 | 20% |
Student > Bachelor | 25 | 15% |
Student > Ph. D. Student | 23 | 14% |
Student > Master | 18 | 11% |
Professor | 6 | 4% |
Other | 27 | 16% |
Unknown | 34 | 20% |
Readers by discipline | Count | As % |
---|---|---|
Biochemistry, Genetics and Molecular Biology | 30 | 18% |
Neuroscience | 30 | 18% |
Agricultural and Biological Sciences | 27 | 16% |
Medicine and Dentistry | 18 | 11% |
Pharmacology, Toxicology and Pharmaceutical Science | 9 | 5% |
Other | 15 | 9% |
Unknown | 38 | 23% |