Isoflavones (ISOs) are naturally occurring endocrine-disrupting compounds. Few human studies have evaluated the effects of ISO exposure on neonatal anthropometry. This study aimed to examine the associations of maternal soy product consumption and urinary ISO concentrations, including genistein, daidzein, glycitein, and equol, with neonatal anthropometry, based on a Chinese cohort study. In Shanghai-Minhang Birth Cohort Study, pregnant women at 12–16 weeks of gestation were recruited, and they completed a structured questionnaire to assess soy product consumption during pregnancy. They also provided a single spot urine sample for the ISO assay. Neonatal anthropometric indices (birth weight; arm, waist, and head circumference; and triceps, back, and abdominal skinfold thickness) were measured at birth. Multivariable linear regression analysis was performed among the 1188 mother-infant pairs to examine the associations between maternal soy product consumption and neonatal anthropometry. The same statistical model was applied to examine the associations between maternal ISO exposure and neonatal anthropometry among 480 mother-infant pairs. Neonate girls born to mothers who “sometimes” and “frequent” consumed soy products had 169.1 g (95% confidence interval [CI], −68.9–407.1) and 256.5 g (95% CI, 17.1–495.8) higher birth weight, respectively, than those born to mothers who “never” consumed soy products during pregnancy. We observed consistent associations between higher maternal urine ISO concentrations and increased anthropometric indices (birth weight, arm and waist circumference, and triceps and abdominal skinfold thickness) in neonate girls, while no association was observed among boys. The findings suggested that maternal dietary ISO intake during pregnancy is associated with fetal development in a sex-specific pattern. In addition, follow-up studies are required to evaluate whether the observed changes in anthropometric indices at birth are associated with health conditions later in life.

Developing therapies for neurodegenerative diseases are challenging because of the presence of blood–brain barrier and Alzheimer being one of the commonest and uprising neurodegenerative disorders possess the need for developing novel therapies. Alzheimer’s is attributed to be the sixth leading cause of death in the USA and the number of cases is estimated to be increased from 58 million in 2021 to 88 million by 2050. Natural drugs have benefits of being cost-effective, widely available, fewer side effects, and immuno-booster can be useful in managing Alzheimer. Flavonoids can slow the neuronal degeneration as they have shown activity in central nervous system and are able to cross the blood–brain barrier. These can be easily extracted from fruits, vegetable, and plants. In Alzheimer disease, flavonoids scavenges the reactive oxygen species and reduces the production of amyloid beta protein. Agents from sub-classes of flavonoids such as flavanones, flavanols, flavones, flavonols, anthocyanins, and isoflavones having pharmacological action in treating Alzheimer disease are discussed in this review.

Long-term exposure to environmental neurotoxic metals is implicated in the induction of dementia and cognitive decline. The present study aims to illustrate the therapeutic role of ipriflavone as a synthetic isoflavone against environmental metal–induced cognitive impairment in rats. Dementia was induced by a mixture of aluminum, cadmium, and fluoride for 90 days followed by ipriflavone for a further 30 days. Metal-treated animals exhibited abnormal behaviors in the Morris water maze task. Neuropathological biomarkers including oxidative stress (TBARS, NO, SOD, GPX, GST, and GSH), inflammation (TNF- α, IL-6, and IL-1β), neurotransmission (AChE and MAO), and insulin resistance (insulin, insulin receptor, and insulin-degrading enzyme) were altered, which consequently elevated the level of amyloid-β42 and tau protein in the hippocampus tissues inducing neuronal injury. Ipriflavone significantly (P < 0.05) ameliorated the neurobehavioral abnormalities and the cognitive dysfunction biomarkers via antioxidant/anti-inflammatory mechanism. Moreover, ipriflavone downregulated the mRNA expression level of amyloid precursor protein and tau protein, preventing amyloid plaques and neurofibrillary tangle aggregation at P < 0.05. A molecular docking study revealed that ipriflavone has a potent binding affinity towards AChE more than donepezil and acts as a strong AChE inhibitor. Our data concluded that the therapeutic potential of ipriflavone against dementia could provide a new strategy in AD treatment.

Oxidative stress and neuroinflammatory changes appear to be the early events involved in AD’s development and progression. The present study was designed to assess the effect of soybean isoflavone extract (SIFE) against colchicine-induced cognitive dysfunction and oxidative stress in male rats.Fifty adult male Wistar albino rats were divided into five groups: control, ACSF-treated group, soybean isoflavones (SIF)-treated group, colchicine (COL)-treated group, and SIF + COL-treated group. We found that an intracerebroventricular (icv) injection of a single dose of colchicine (7.5 μg/rat bilaterally) resulted in learning deficits in rats subjected to the Morris water maze task associated with marked oxidative damage and decreased acetyl cholinesterase (AChE) activity. In addition, COL caused significant increase in amyloid beta peptide 1-42 (β, amyloid 1-42) interleukin-1β (IL-1β), tumor necrosis factor-α (TNFα), cyclooxygenase-2 (COX-2) and TNF-α genes expression in the brain, and glial fibrillary acidic protein (GFAP) in cortical astrocytes in the brain cortex.Treatment with SIFE (80 mg/kg b.wt) daily for 14 days followed by a single dose of COL significantly reduced the elevated oxidative stress parameters and restored the reduced antioxidant activities. Besides, the administration of SIFE reversed the overproduction of β, amyloid 1-42, pro-inflammatory cytokines, and GFAP in the brain. The obtained results were confirmed by histological observations that clearly indicate a neuroprotective effect of SIF against AD.