Cholesterol homeostasis in neurons and glial cells
Seminars in Cell & Developmental Biology, ISSN: 1084-9521, Vol: 16, Issue: 2, Page: 193-212
2005
- 173Citations
- 161Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations173
- Citation Indexes170
- 170
- CrossRef126
- Policy Citations3
- Policy Citation3
- Captures161
- Readers161
- 161
Review Description
Cholesterol is highly enriched in the brain compared to other tissues. Essentially all cholesterol in the brain is synthesized endogenously since plasma lipoproteins are unable to cross the blood–brain barrier. Cholesterol is transported within the central nervous system in the form of apolipoprotein E-containing lipoprotein particles that are secreted mainly by glial cells. Cholesterol is excreted from the brain in the form of 24-hydroxycholesterol. Apolipoprotein E and cholesterol have been implicated in the formation of amyloid plaques in Alzheimer's disease. In addition, the progressive neurodegenerative disorder Niemann-Pick C disease is characterized by defects in intracellular trafficking of cholesterol.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S1084952105000212; http://dx.doi.org/10.1016/j.semcdb.2005.01.005; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=15944389528&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/15797830; https://linkinghub.elsevier.com/retrieve/pii/S1084952105000212; https://dx.doi.org/10.1016/j.semcdb.2005.01.005
Elsevier BV
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