While this blog usually focuses on joint restoration, pain relief for the arthritic joint and improved functional capacity, I have condensed a recently published article as it would seem there is increasing need to stay active and I can assist those limited by arthritis.
An international team of researchers representing several institutions in Japan and the United States has published promising findings that may stand to benefit people living with the specter of Alzheimer’s and other neurodegenerative diseases, as well as age-related cognitive decline.
In their paper published in PNAS, “Leptin in hippocampus mediates benefits of mild exercise by an antioxidant effect on neurogenesis and memory,” Yook and colleagues present results from a series of experiments—murine and in vitro—that elucidate the role of leptin in cognitive function. Leptin is a hormone that is produced in adipose tissue and in the hippocampus, the part of the brain where memory and spatial learning are processed.
The relationship between exercise and improved cognitive function is well established. Likewise, certain dietary supplements, for example, docosahexaenoic acid (DHA) have also shown promise in improving cognition and in slowing or halting cognitive decline. The effect of both exercise and supplementation with an antioxidant on plasticity and cognitive function within the hippocampus has until now been largely unexplored, however. Previous research has demonstrated that leptin in particular is a promising therapeutic target for neurodegenerative diseases such as Alzheimer’s.
Yook and colleagues sought to answer the particular question of whether mild exercise (ME) combined with the antioxidant supplement astaxanthin (AX) might confer benefit in terms of cognitive function and neuronal plasticity; and whether or not the two interventions—AX and ME together—could have a synergistic effect beyond the additive effects of either treatment administered separately. The investigators “hypothesized that ME-enhanced hippocampal neurogenesis and memory might be further improved with dietary AX via mediation by a neurotrophic factor such as h-LEP [hippocampal leptin].”.
For the in vitro experiment, the investigators used human neuroblastoma cell lines—cells known to endogenously synthesize leptin—to observe the effect of exposing them.
While the results shown here in murine models are certainly promising, what might this mean in a clinical context for humans? For one thing, mild exercise for humans has been characterized in this paper as that which is typical of a yoga or tai chi session, which puts it within reach of many people. Another factor is the ready availability of the relatively inexpensive nutritional supplement astaxanthin.
Ultimately, the authors conclude that “our findings advance the notion that ME combined with a dietary antioxidant such as AX, which induces endogenous h-LEP, may be an effective nonpharmacological strategy for preventing or improving cognitive function and brain health, and for slowing cognitive decline. This strategy may be particularly useful in vulnerable individuals, including the elderly.”
In simple terms, get plenty of rest, plenty of exercise and take the nutritional supplement astaxanthin. If injury or an arthritic joint prevent you from mild or even a full recreational profile, schedule a consultation by calling (847) 390-7666. You may visit my website at sheinkopmd.com.