ID differentially alters dendritic arbor pattern and length of hippocampal dendrites

Here we focus on Iron Deficiency (ID), which is the most prevalent nutritional deficiency worldwide and affects mainly pregnant women and children. While it is well established that gestational ID causes a number of neurological problems in the offspring that cannot be treated with postnatal supplementation, the cellular targets, mechanisms of action and time of greatest vulnerability to fetal brain development remain elusive. One major obstacle that hindered insight into the impact of ID is the often co-occurring anemia, which makes it difficult to distinguish the impact of low iron from that of anemia-associated issues. We established a unique animal model in mice and rats of gestational ID that is defined by fetal tissue iron depletion in the absence of maternal anemia. This animals model system allowed us to separate the effects of ID on brain cells from those caused by anemia. Using non-invasive auditory brain stem response analysis as a tool to identify global brain maturation defects we identified the vulnerable window during which ID affects the neural development in the offspring. We are now in the process of defining the cellular targets of ID in the fetal brain and the mechanisms by which ID affects these vulnerable neural cell populations.

ID impairs axon maturation of the auditory nerve

Window of vulnerability