ABSTRACT
Iron deficiency is a recognized global health concern, particularly impactful during pregnancy where the mother serves as the primary source of iron for the developing fetus. Adequate maternal iron levels are crucial for fetal growth and cognitive development. This review investigates the correlation between maternal iron deficiency and cognitive impairment and anemia in offspring, considering age and gender differentials. PubMed, ScienceDirect, and Google Scholar databases were queried using keywords "maternal," "iron," "gender/sex," and "cognition." The review included studies on human and animal subjects where maternal iron deficiency was the exposure and offspring cognitive function and anemia were outcomes. Out of 1139 articles screened, fourteen met inclusion criteria. Twelve studies highlighted cognitive deficits in offspring of iron-deficient mothers, with females generally exhibiting milder impairment compared to males. Additionally, two studies noted increased anemia prevalence in offspring of iron-deficient mothers, particularly affecting males and younger individuals. The findings suggest that male offspring are at higher risk of both anemia and cognitive dysfunction during youth, while females face increased risks in adulthood. Thus, maternal iron deficiency elevates the likelihood of anemia and cognitive impairments in offspring, underscoring the importance of addressing maternal iron status for optimal child health.
Subject(s)
Anemia, Iron-Deficiency , Cognition , Iron Deficiencies , Humans , Female , Pregnancy , Anemia, Iron-Deficiency/epidemiology , Anemia, Iron-Deficiency/blood , Male , Prenatal Exposure Delayed Effects , Sex Factors , Animals , Maternal Nutritional Physiological Phenomena , Age Factors , Pregnancy Complications , Cognitive Dysfunction/etiology , Cognitive Dysfunction/epidemiology , Iron/blood , ChildABSTRACT
Traumatic brain injury (TBI) remains a public health challenge and represents one of the major contributors to disability and mortality worldwide among all trauma-related injuries. This study aimed to determine a precise effect size of secretome intervention in TBI. We performed a systematic literature search through Cochrane, MEDLINE Complete, PubMed and Scopus databases for articles published until June 2021. The search terms used include cells OR stem cells OR mesenchymal stem cells AND secretome OR conditioned medium OR extracellular vesicles OR exosomes OR microvesicles AND traumatic brain injury OR head injury. Neurological deficits and neuroinflammation were the outcome measures assessed after the intervention. Thirty-one (31) studies involving mouse, rat and swine were enrolled for the meta-analysis. Secretome significantly improved structural and functional recovery when compared with control. The mean effect sizes were as follows: modified neurological severity score (mNSS) (-2.65, 95% CI: -3.42, -1.87, p < 0.00001), impact size (-3.02 mm3, 95% CI: -4.97, -1.08, p = 0.002) and latency to platform (-17.20 s, 95% CI: -23.91, -10.50, p < 0.00001). Similarly, intervention with secretome reduced neuroinflammation after TBI. The results of meta-regression showed that the source of secretome, TBI models and duration of follow-up did not influence the mNSS. Furthermore, the methodological quality of the studies was moderate as shown by the risk of bias assessment. Publication bias was observed for the mNSS. This meta-analysis provides preclinical evidence of secretome intervention in TBI, suggesting that it can be explored as a therapeutic agent for TBI and other neurological disorders in humans.
