Early-Stage Discoveries: Curcumin, Prebiotics, and L-Serine
Good results in the lab can lead to larger human trials. Here are some of the most promising recent findings.
Curcumin cut inflammation linked to memory loss
Curcumin is a well-known anti-inflammatory. Specialized immune nerve cells in the brain and spinal cord, called microglia, clean up the amyloid plaques that accumulate in Alzheimer’s disease (AD). But inflammatory proteins can damage microglia. In the lab, microglia cells treated with curcumin released far lower levels of this inflammatory protein, HMGB1, compared to untreated cells.
Doctors said the results suggest that curcumin can effectively inhibit nerve cell inflammation, and that this study reveals curcumin’s anti-inflammatory method of action.
Reference: Annals of Translational Medicine; February, 2020, Vol. 8, No. 4
Prebiotics improve sleep, stress resilience
Prebiotics can influence bodily functions including sleep and recovering from stress. In the lab, doctors added prebiotics to the diets of rats and found, compared to those that didn’t get prebiotics, they spent more time in restorative, non-rapid-eye-movement (NREM) sleep, and after stress, spent more time in REM sleep, which is crucial for recovering from stress. Also, the prebiotics group retained daily, healthy, natural body temperature fluctuations, and greater diversity of healthy gut bacteria. Doctors concluded prebiotics can buffer against stress.
Reference 2: Nature – Scientific Reports; 2020, Vol. 10, Article No. 3848
L-serine restored memory
Doctors have discovered a metabolic pathway that converts glucose to energy may play a role in Alzheimer’s disease (AD). Special cells called astrocytes use glucose to produce an amino acid, L-serine, which feeds nearby nerve-cell receptors essential for brain function and memory. But when astrocytes use less glucose, L-serine levels decline, damaging nerves and memory capacity.
In the lab, doctors restored the capacity for memorization functions in mice fed L-serine, which suggests L-serine may complement treatments for early symptoms of AD, Parkinson’s, and Huntington’s diseases.
Reference 3: Cell Metabolism; 2020, Vol. 31, No. 3, 503-17