Microglia are the brain's resident immune cells that respond to injury and disease by transitioning between homeostatic and reactive states. These cell state transitions determine whether microglia pr Show more
Microglia are the brain's resident immune cells that respond to injury and disease by transitioning between homeostatic and reactive states. These cell state transitions determine whether microglia promote or resolve inflammation in the central nervous system (CNS). In this study, we explored the role of Ca Show less
One hundred participants aged 40-65 with subjective complaints of poor memory were randomized into two groups: 300 mg of LN19184 or placebo, once daily for 120 days. At baseline and days 15, 30, 60, a Show more
One hundred participants aged 40-65 with subjective complaints of poor memory were randomized into two groups: 300 mg of LN19184 or placebo, once daily for 120 days. At baseline and days 15, 30, 60, and 120, two neuropsychological batteries, the Rey's Auditory Verbal Learning Test (RAVLT) and the Cambridge Neuropsychological Test (CANTAB), were used to assess cognitive function, and the Athens Insomnia Scale was used to evaluate sleep quality. Serum BDNF levels and safety parameters were also assessed. LN19184 improved each measured RAVLT outcome compared to placebo. Supplementation improved proactive interference ( This pilot trial provides early empirical evidence demonstrating that a novel extract blend of Clinicaltrials.gov, identifier CTRI/2020/08/027368. Show less
The nutritional environment encountered during fetal life is strongly implicated as a determinant of lifelong metabolic capacity and risk of disease. Pregnant rats were fed a control or low-protein (L Show more
The nutritional environment encountered during fetal life is strongly implicated as a determinant of lifelong metabolic capacity and risk of disease. Pregnant rats were fed a control or low-protein (LP) diet, targeted to early (LPE), mid-(LPM), or late (LPL) pregnancy, or throughout gestation (LPA). The offspring were studied at 1, 9, and 18 mo of age. All LP-exposed groups had similar plasma triglyceride, cholesterol, glucose, and insulin concentrations to those of controls at 1 and 9 mo of age, but by 18 mo there was evidence of LP-programmed hypertriglyceridemia and insulin resistance. All LP-exposed groups exhibited histological evidence of hepatic steatosis and were found to have two- to threefold more hepatic triglyceride than control animals. These phenotypic changes were accompanied by age-related changes in mRNA and protein expression of the transcription factors SREBP-1c, ChREBP, PPARgamma, and PPARalpha and their respective downstream target genes ACC1, FAS, L-PK, and MCAD. At 9 mo of age, the LP groups exhibited suppression of the SREBP-1c-related lipogenic pathway but between 9 and 18 mo underwent a switch to increased lipogenic capacity with a lower expression of PPARgamma and MCAD, consistent with reduced lipid oxidation. The findings indicate that prenatal protein restriction programs development of a metabolic syndrome-like phenotype that develops only with senescence. The data implicate altered expression of SREBP-1c and ChREBP as key mediators of the programmed phenotype, but the basis of the switch in metabolic status that occurred between 9 and 18 mo of age is, as yet, unidentified. Show less