"Interferon-gamma is up-regulated in the hippocampus in response to intermittent fasting and protects hippocampal neurons against excitotoxicity."
http://www.ncbi.nlm.nih.gov/pubmed/16521127Luckily through my immunology studies, and since IFN-gamma is a Th1 based cytokine, I spent many a time cracking this nut. The upregulation is likely via the increase in CREB through fasting due to norepinephrine, glucagon, etc. CREB allows an adequate expression of Egr, which then upregulates TBX21 (T-bet) and that mediates the increase in IFN-gamma levels, as does the effects of CREB itself, albeit it that's much more subtle as CREB usually does it's work in concert with like ATF-1, NFAT, and so on.
This is pretty interesting though. However, I somewhat disagree with their surmise of a hormetic effect mediating this upregulation. It can be perfectly explained without it.
"Signalling through RHEB-1 mediates intermittent fasting-induced longevity in C. elegans."
http://www.ncbi.nlm.nih.gov/pubmed/19079239Not sure what to make of this one. It's just an interesting interaction between the RHEB-TOR system
"Adaptation to intermittent fasting as a factor modifying the radiation resistance of mice"
http://www.researchgate.net/publication/226283394_Adaptation_to_intermittent_fasting_as_a_factor_modifying_the_radiation_resistance_of_miceI can hardly view any text of this one, however, from the few sentences of the abstract it seems to corroborate what I've said of mitohormesis and IF. It induces a hormetic effect, which then also augments stress resistance to all stressors, which this demonstrates.
"Neuroprotective role of intermittent fasting in senescence-accelerated mice P8 (SAMP8)."
http://www.ncbi.nlm.nih.gov/pubmed/20460146They basically show that IF increases Sirt1 expression, as expected, to increase life-span. They also noted increase levels of HSP70 (heat shock protein), further corroborating the fact that IF induces mitohormesis, plus an elevation in BDNF, as expected.