Neural evidence for the use of digit-image mnemonic in a superior memorist: An fMRI study

Some superior memorists demonstrated exceptional memory for reciting a large body of information. The underlying neural correlates, however, are seldom addressed. C.L., the current holder of Guinness World Record for reciting 67,890 digits in π, participated in this functional magnetic resonance imaging (fMRI) study. Thirteen participants without any mnemonics training were included as controls. Our previous studies suggested that C.L. used a digit-image mnemonic in studying and recalling lists of digits, namely associating 2-digit groups of ‘00’ to ‘99’ with images and generating vivid stories out of them (Hu, Ericsson, Yang & Lu, 2009). Thus, 2-digit condition was included, with 1-digit numbers and letters as control conditions. We hypothesized that 2-digit condition in C.L. should elicit the strongest activity in the brain regions which are associated with his mnemonic. Functional MRI results revealed that bilateral frontal poles (FPs, BA10), left superior parietal lobule (SPL), left premotor cortex (PMC), and left dorsolateral prefrontal cortex (DLPFC), were more engaged in both the study and recall phase of 2-digit condition for C.L. relative to controls. Moreover, the left middle/inferior frontal gyri (M/IFG) and intraparietal sulci (IPS) were less engaged in the study phase of 2-digit condition for C.L. (vs. controls). These results suggested that C.L. relied more on brain regions that are associated with episodic memory other than verbal rehearsal while he used his mnemonic strategies. This study supported theoretical accounts of restructured cognitive mechanisms for the acquisition of superior memory performance

Intranasal deferoxamine attenuates synapse loss via up-regulating the P38/HIF-1α pathway on the brain of APP/PS1 transgenic mice

AbstractThe widely recognized neuroprotective effect of iron chelators is contributed by their ability to prevent reactive oxygen species generation via the Fenton reaction, which sequesters redox-active Fe. An additional neuroprotective mechanism of iron-chelating compounds is to regulate the transcriptional activator hypoxia-inducible factor 1α (HIF-1α). In the present study, we observed that intranasal administration of deferoxamine decreased beta-amyloid (Aβ) deposition and rescued synapse loss in the brain of Aβ precursor protein and presenilin-1 (APP/PS1) double transgenic mice. We found that DFO up-regulated HIF-1α mRNA expression and its protein level, and further induced the proteins that are encoded from HIF-1-adaptive genes, including transferrin receptor (TFR), divalent metal transporter 1 (DMT1), and brain-derived neurotrophic factor (BDNF). The effects of DFO on the induction and stabilization of HIF-1α were further confirmed in vitro. This was accompanied by a decrease of Fe in the CA3 region of the hippocampus. Western blotting studies revealed that DFO differentially enhanced the phosphorylation of mitogen-activated protein kinase (MAPK) /P38 kinase in vitro and in vivo. The results suggest that the DFO may up-regulate several HIF-1-dependent neuroprotective-adaptive genes in AD via activating P38/HIF-1α pathway, which may serve as important therapeutic targets to the disease