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ISMCBBPR's Molecule of the Year 2012 and the Runners- Up
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- Molecule of the Year  2012 and the runners up & the voters’ statements (marked with ~~)

Molecule of the Year 2012 is the DESMOSTEROL

~~Strong evidence is presented in the accompanying article that shows how this appears to be a prime regulator of inflammatory genes at multiple pathways and that it has or synthetic derivatives of it have the potential to be useful in inhibiting the inflammatory response for the treatment of cardiovascular diseases.

~~My choice for Molecule of the year, 2012 is Desmosterol. This molecule, which is a precursor of cholesterol is involved in maintaining homeostasis in a large number of tissues. While it plays a major role during mammalian brain development, it is important for regulation of inflammatory responses. Recent contributions made for the understanding of primary functions of this molecule have shown that maintaining desmosterol-cholesterol balance is necessary for homeostasis. It is also important in the control of a variety of human disorders.


Regulated accumulation of desmosterol integrates macrophage lipid metabolism and inflammatory responses. 2012.Spann NJ, Garmire LX, McDonald JG, Myers DS, Milne SB, Shibata N, Reichart D, Fox JN, Shaked I, Heudobler D, Raetz CR, Wang EW, Kelly SL, Sullards MC,Murphy RC, Merrill AH Jr, Brown HA, Dennis EA, Li AC, Ley K, Tsimikas S, Fahy E, Subramaniam S, Quehenberger O, Russell DW, Glass CK. Cell. 2012 Sep 28;151(1): 138-52.doi: 10.1016/j.cell.2012.06.054  PMID: 23021221  [PubMed - indexed for MEDLINE] PMCID: PMC3464914

1st Runner Up:


~~Very interesting discovery of the close homolog of BACE1 which is involved in the production of beta-amyloid. BACE2 is actually a very strong beta-amyloid degrading enzyme. It thus represents a new and strong candidate for therapies to treat / prevent Alzheimer's disease.

~~This molecule provides hope for treatment of patients with neurological disorders like Alzheimer's and Down's.


Identification of BACE2 as an avid ß-amyloid-degrading protease.2012.Abdul-Hay SO, Sahara T, McBride M, Kang D, Leissring MA. Mol Neurodegener.2012 Sep 17;7:46. doi: 10.1186/1750-1326-7-46 PMID: 22986058 [PubMed - indexed for MEDLINE] PMCID: PMC3470943


2nd Runner Up:


~~Population studies have earlier shown an association of mutations in Nlgn3 to be associated with autism  in various ethnic groups. Animal studies also validate the role of Nlgn3 mutations in causing autism- like phenotype indicating clearly that Nlgn3 is important as a cell adhesion molecule to maintain proper synapses.


Shared synaptic pathophysiology in syndromic and nonsyndromic rodent models of autism. 2012. Baudouin SJ1, Gaudias J, Gerharz S, Hatstatt L, Zhou K, Punnakkal P, Tanaka KF, Spooren W, Hen R, De Zeeuw CI, Vogt K, Scheiffele P. Science. 2012 Oct 5;338(6103):128-32. doi: 10.1126/science.1224159. Epub 2012 Sep 13.PMID: 22983708  [PubMed - indexed for MEDLINE]