Issue 4, 2006

For some reason, this issue is free so I can read any articles I feel interested in, but since I don't really have any time to read papers, I will stick mostly to the abstracts.

There is a series of comment articles that are followups to the Special Interest Group on Societal Implications of Anti-Aging Research at the the 2005 Gerontology Society of America's conference discussing the usual SENS vs nonSENS.

"Site-Specific Integration into the Human Genome: Ready for Clinical Application?". A commentary piece on the possibilities of practical use of adeno-associated virus (AAV) for clinical gene insertion. AAV can insert its genome into a specific part of chromosome 19 (AAVS1), but it can only carry a very small payload. To enlarge the payload it's usually used without the site-specific integration gene (Rep) which ruins the reason for using AAV in the first place. What was new work at the time was a development of a hybrid between the herpes simplex virus and AAD to keep the site-specific integration while enlarging the payload and not overdoing the Rep expression which otherwise causes problems. Article says it isn't good enough for the clinic yet because the site-specificity isn't good enough (70%) and because of low efficiency of gene transfer which they claim to be 20% for stable cell lines (my problem here is that I don't know what the efficiency means. That 20% of the cells get the gene inserted into them sounds like the most likely meaning).

"Mitochondrial Transfer Between Eukaryotic Animal Cells and Its Physiologic Role". Another commentary piece on a paper that appeared in PNAS reporting the rescue of cells grown without mtDNA when grown among normal human skin fibroblasts and mesenchymal stem cells in vitro. By rescue, they mean that after a while, the sans-mtDNA cells appear to acquire functional mitochondrial and they multiply as normal. The commentary is on the mechanism of mitochondrial transfer and on whether the usual function of mitotransfer is that good mitochondria flow from good cells to bad cells or the reverse, the first one as an analogy to entropy, the second seeing mitochondria as selfish agents. The author prefers the first option.

"Expression of Algal Nuclear ATP Synthase Subunit 6 in Human Cells Results in Protein Targeting to Mitochondria but No Assembly into ATP Synthase" by M Bokori-Brown and IJ Holt. Very interesting and thorough attempt at introducing a version of the human subunit a (A6) of ATP synthase gene into a human cell's nuclear DNA. They tried many versions and the one that targeted to the mitochondria best was a version from an algae (Chlamydomonas reinhardtii) that is naturally in the nDNA, with various hybrids working less well. The problem is that the better the protein was targetted, the worse the cell did. Some more imagery shows that the protein doesn't colocalise with the ATP synthase on the mitochondria, so it's just gunking up the mitochondria, not doing anything useful.

"Erythrocyte Plasma Membrane Redox System in Human Aging" by SI Rizvi, R Jha and PK Maurya. Correlation of 0.78 between the level of export of electrons by red blood cells through the plasma membrane redox system, and age in 80 people. Similar inverse correlation between plasma antioxidant capacity and age.

"Selegiline Induces Neuronal Phenotype and Neurotrophins Expression in Embryonic Stem Cells" by F Esmaeili, T Tiraihi, M Movahedin and SJ Mowla. What the title says.

"VEGF Gene and Phenotype Relation with Alzheimer's Disease and Mild Cognitive Impairment" by M Chiappelli, B Borroni, S Archetti, E Calabrese, MM Corsi, M Franceschi, A Padovani and F Licastro. Link between a variant in the vascular enthelial growth factor (VEGF) gene promoter and Alzheimer's and mild cognitive impairment in a study of about 1000 people total. AA variant were 1.6 times more common than expected among AD. Also deteriorated fast 6 times more often if they had an ApoE4 allele. AA variant had more VEGF in circulation.