@article {316360,
	title = {The Alzheimer{\textquoteright}s disease{\textendash}protective CD33 splice variant mediates adaptive loss of function via diversion to an intracellular pool},
	journal = {J Biol Chem},
	volume = {292},
	year = {2017},
	note = {<p>Times cited: 1</p>
},
	pages = {15312-15320},
	abstract = {<p>The immunomodulatory receptor Siglec-3/CD33 influences risk for late-onset Alzheimer{\textquoteright}s disease (LOAD), an apparently human-specific post-reproductive disease. CD33 generates two splice variants: a full-length CD33M transcript produced primarily by the {\textquotedblleft}LOAD-risk{\textquotedblright} allele and a shorter CD33m isoform lacking the sialic acid-binding domain produced primarily from the {\textquotedblleft}LOAD-protective{\textquotedblright} allele. An SNP that modulates CD33 splicing to favor CD33m is associated with enhanced microglial activity. Individuals expressing more\&nbsp;{\textellipsis}</p>
},
	url = {http://www.jbc.org/content/292/37/15312.full},
	author = {Siddiqui, SS and Springer, SA and Verhagen, A and Sundaramurthy, V and Alisson-Silva, F and Jiang, W and Ghosh, P and Ajit Varki}
}
