A recent study in Rejuvenation Research reports that a combination of dietary supplements confer neuroprotection in stroke. Over a 2 week period rats received either a proprietary formulation of blueberry, green tea, Vitamin D3, and carnosine called NT-020 or vehicle (i.e., the same solution minus the compounds of interest) before stroke was induced through middle cerebral artery occlusion (MCAo). Two weeks after the insult the rats were subjected to behavioral tests and histological examination. Rats treated with the dietary supplements scored better on behavioral tests, had less histological damage, and showed evidence of neurogenesis.
This study is interesting for a number of reasons. Foremost, it highlights the possibility that dietary choices can positively affect outcome after ischemic insults. These findings complement research that found that caloric restriction improves behavioral and histological outcome after stroke. The findings also reinforce that some of the most effective neuroprotective agents to date are ordinary nutrients, vitamins, and hormones. In this study the investigators combine a number of these agents to greater effect. Although the authors do not present specific data on bioavailability in the brain for these compounds, they argue that a multi-agent approach relaxes the dosage requirements for individual agents.
The paper reviews assays that demonstrate improved neurogenesis in the rats that received NT-020 such as endogenous birth of new neurons, neuronal phenotype expression of newly formed cells, and alterations in neurogenic factors. Pharmacological modulation of neurogenesis after ischemia is a young research field and the results reported in this paper provide additional evidence for the (only recently accepted) phenomenon of adult neurogenesis. Unresolved questions at this point include how neurogenesis differs among species and whether post-ischemic neurogenesis can improve long term outcome in humans.
The design of the current study does not allow a rigorous answer to the question of whether neurogenesis contributed to or accompanied improved outcome. The possibility that other mechanisms (such as increased free radical scavenging) were primarily responsible for the observed improvements cannot be ruled out based on this study.