Abstract
Resilience after 3/11: structural brain changes 1 year after the Japanese earthquake.
Highlights
A recent investigation by our lab identified regional grey matter volume changes in people in the months following the Japanese earthquake.[3]. These findings indicated that smaller anterior cingulate cortex volume was a preexisting vulnerability factor for posttraumatic stress disorder (PTSD) symptoms and that decreased volume of the orbitofrontal cortex (OFC) was a result of these acquired symptoms.[3]
Post hoc correlation analyses revealed that the increase in the volume of the left OFC from Post to Follow-up was significantly correlated with self-esteem scores at Post (r = 0.43, P = 0.007; Supplementary Table S3)
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Summary
552 clearly distinguished from the other samples analyzed, and displayed a 1.5–2-fold greater increase in cell number, mainly at the later time points of the curve (Figure 1b, Supplementary Figure 1b), and reduced response to the antiproliferative effect of rapamycin, a specific mTOR inhibitor (Figure 1c, Supplementary Figure 1c). Whereas dual PI3K-mTOR inhibition (wortmannin+rapamycin treatment) continued to be less effective in reducing to a similar extent the proliferation of ASD1–2 and control cells, it was able to restore the enhanced proliferation of ASD3 cells (Figure 1c, Supplementary Figure 1c), suggesting a possible different regulatory mechanism in ASD3 cells. Knockout mouse models of both syndromic and nonsyndromic ASD with disinhibited mTOR signaling and dysregulated protein synthesis present dysplastic and enlarged neurons with increased spine density in several brain regions.[5,7,8] we did not notice increased ASD1–3 SHED volumes, it will be important to determine and explore further whether the altered proliferative phenotype observed in these cells may be observed in neuronal cell types, which could be a potential additional mechanism whereby disrupted mTORC1 signaling contributes to ASD neuropathology. Our results suggest that SHEDs are an alternative and more readily accessible source of patient material to study disease pathophysiology and to refine treatment approaches for individual patients
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