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Item Building a surface atlas of hippocampal subfields from high resolution T2-weighted MRI scans using landmark-free surface registration(IEEE, 2016-10) Cong, Shan; Rizkalla, Maher; Salama, Paul; Electrical and Computer Engineering, School of Engineering and TechnologyThe hippocampus is widely studied in neuroimaging field as it plays important roles in memory and learning. However, the critical subfield information is often not explored in most hippocampal studies. We previously proposed a method for hippocampal subfield morphometry by integrating FreeSurfer, FSL, and SPHARM tools. But this method had some limitations, including the analysis of T1-weighted MRI scans without detailed subfield information and hippocampal registration without using important subfield information. To bridge these gaps, in this work, we propose a new framework for building a surface atlas of hippocampal subfields from high resolution T2-weighted MRI scans by integrating state-of-the-art methods for automated segmentation of hippocampal subfields and landmark-free, subfield-aware registration of hippocampal surfaces. Our experimental results have shown the promise of the new framework.Item FKBP51 modulates hippocampal size and function in post-translational regulation of Parkin(Springer, 2022-03-04) Qiu, Bin; Zhong, Zhaohui; Righter, Shawn; Xu, Yuxue; Wang, Jun; Deng, Ran; Wang, Chao; Williams, Kent E.; Ma, Yao-ying; Tsechpenakis, Gavriil; Liang, Tiebing; Yong, Weidong; Surgery, School of MedicineFK506-binding protein 51 (encoded by Fkpb51, also known as Fkbp5) has been associated with stress-related mental illness. To investigate its function, we studied the morphological consequences of Fkbp51 deletion. Artificial Intelligence-assisted morphological analysis revealed that male Fkbp51 knock-out (KO) mice possess more elongated dentate gyrus (DG) but shorter hippocampal height in coronal sections when compared to WT. Primary cultured Fkbp51 KO hippocampal neurons were shown to exhibit larger dendritic outgrowth than wild-type (WT) controls and pharmacological manipulation experiments suggest that this may occur through the regulation of microtubule-associated protein. Both in vitro primary culture and in vivo labeling support a role for FKBP51 in the regulation of microtubule-associated protein expression. Furthermore, Fkbp51 KO hippocampi exhibited decreases in βIII-tubulin, MAP2, and Tau protein levels, but a greater than 2.5-fold increase in Parkin protein. Overexpression and knock-down FKBP51 demonstrated that FKBP51 negatively regulates Parkin in a dose-dependent and ubiquitin-mediated manner. These results indicate a potential novel post-translational regulatory mechanism of Parkin by FKBP51 and the significance of their interaction on disease onset.Item Gene expression changes in the ventral hippocampus and medial prefrontal cortex of adolescent alcohol-preferring (P) rats following binge-like-alcohol drinking(Elsevier, 2017) McClintick, Jeanette N.; McBride, William J.; Bell, Richard L.; Ding, Zheng-Ming; Liu, Yunlong; Xuei, Xiaoling; Edenberg, Howard J.; Biochemistry and Molecular Biology, School of MedicineBinge drinking of alcohol during adolescence is a serious public health concern with long-term consequences, including decreased hippocampal and prefrontal cortex volume and defects in memory. We used RNA sequencing to assess the effects of adolescent binge drinking on gene expression in these regions. Male adolescent alcohol-preferring (P) rats were exposed to repeated binge drinking (three 1-hour sessions/d during the dark/cycle, 5 days/week for 3 weeks starting at 28 days of age; ethanol intakes of 2.5 to 3 g/kg/session). Ethanol significantly altered the expression of 416 of 11,727 genes expressed in the ventral hippocampus. Genes and pathways involved in neurogenesis, long-term potentiation and axonal guidance were decreased, which could relate to the impaired memory function found in subjects with adolescent alcohol binge-like exposure. The decreased expression of myelin and cholesterol genes and apparent decrease in oligodendrocytes in P rats could result in decreased myelination. In the medial prefrontal cortex, 638 of 11,579 genes were altered; genes in cellular stress and inflammatory pathways were increased, as were genes involved in oxidative phosphorylation. Overall, the results of this study suggest that adolescent binge-like alcohol drinking may alter the development of the ventral hippocampus and medial prefrontal cortex and produce long-term consequences on learning and memory, and on control of impulsive behaviors.Item Resting-state fMRI Activity Profile in Prodromal Alzheimer’s Disease and Older Adults with Cognitive Complaints(Office of the Vice Chancellor for Research, 2013-04-05) Wang, Yang; West, John D.; Magee, Tamiko R.; McDonald, Brenna C.; Risacher, Shannon L.; Farlow, Martin R.; O'Neill, Darren P.; Saykin, Andrew J.Background: Resting-state functional MRI (RS-fMRI) has been proposed to detect neurodegenerative disease-related network alterations before brain atrophy has emerged. Disrupted resting-state connectivity in the posterior cingulate cortex (PCC) and hippocampus has been reported in AD (Grecius, 2004), yet results in prodromal AD including MCI vary. Other methods have suggested the feasibility of earlier detection in euthymic older adults with marked cognitive complaints (CC) but normal neuropsychological test performance (Saykin, 2006). The current study was designed to assess RS-fMRI patterns in CC compared with MCI, AD and healthy controls (HC). Methods: To date, 13 CC, 9 HC, 4 MCI and 3 AD participants were scanned at rest with eyes closed on a Siemens 3T. RS-fMRI was analyzed using FSL, AFNI and SPM8. For each individual, the sum of amplitude of low frequency fluctuation (ALFF; 0.01–0.1 Hz) was calculated at each voxel (Biswal, 2010). Using PCC seed ROIs adapted from Fox et al (2005) voxel-wise cross-correlation maps were generated for each subject. Group comparisons and covariate analyses were performed using SPM8 with age as a covariate. Results: Compared to HC, MCI/AD showed decreased ALFF in the PCC (p<0.01, corrected), but increased ALFF in bilateral hippocampi (p<0.01). The CC group consistently showed intermediate changes. ROI analyses indicated differences in ALFF of PCC (HC > CC > MCI/AD, p<0.05, effect size: 0.61), and ALFF of hippocampus (HC < CC < MCI/AD, p<0.01, effect size: 0.75). ALFF of PCC was positively correlated with neuropsychological performance (MMSE, DRS and CVLT; r=0.45 to 0.56, p<0.01), while hippocampal ALFF was negatively correlated with performance (r=-0.48 to -0.67, p<0.01). PCC seeded crosscorrelation maps showed decreased hippocampal connectivity in MCI/AD compared to HC or CC (p<0.01). Conclusions: RS-fMRI appears sensitive to early prodromal neurodegenerative changes in regions associated with AD, notably including pre-MCI individuals with CC. While there is decreased functional connectivity between PCC and hippocampus, regionally increased ALFF in hippocampus may indicate a compensatory mechanism in early prodromal AD.Item Transcriptome Profiling of the Hippocampal Seizure Network Implicates a Role for Wnt Signaling during Epileptogenesis in a Mouse Model of Temporal Lobe Epilepsy(MDPI, 2022-10) Mardones, Muriel D.; Gupta, Kunal; Neurological Surgery, School of MedicineMesial temporal lobe epilepsy (mTLE) is a life-threatening condition characterized by recurrent hippocampal seizures. mTLE can develop after exposure to risk factors such as febrile seizure, trauma, and infection. Within the latent period between exposure and onset of epilepsy, pathological remodeling events occur that contribute to epileptogenesis. The molecular mechanisms responsible are currently unclear. We used the mouse intrahippocampal kainite model of mTLE to investigate transcriptional dysregulation in the ipsilateral and contralateral dentate gyrus (DG), representing the epileptogenic zone (EZ) and peri-ictal zone (PIZ). DG were analyzed after 3, 7, and 14 days by RNA sequencing. In both the EZ and PIZ, transcriptional dysregulation was dynamic over the epileptogenic period with early expression of genes representing cell signaling, migration, and proliferation. Canonical Wnt signaling was upregulated in the EZ and PIZ at 3 days. Expression of inflammatory genes differed between the EZ and PIZ, with early expression after 3 days in the PIZ and delayed expression after 7–14 days in the EZ. This suggests that critical gene changes occur early in the hippocampal seizure network and that Wnt signaling may play a role within the latent epileptogenic period. These findings may help to identify novel therapeutic targets that could prevent epileptogenesis.Item TRAUMATIC BRAIN INJURY LEADS TO ABERRANT MIGRATION OF ADULT-BORN NEURONS IN THE HIPPOCAMPUS(Office of the Vice Chancellor for Research, 2012-04-13) Ibrahim, Sara; Gao, Xiang; Chen, JinhuiTraumatic brain injury (TBI) is the leading cause of death in children and young adults, leading to substantial cognitive impairment, motor dysfunction and epilepsy. There is no effective treatment for these dis-orders. The discovery of neural stem/progenitor cells (NSCs) in the adult brain raises a potentially promising strategy for repairing CNS in-jury.Our previous study showed that TBI promotes NSC proliferation in an attempt to initiate innate repair and/or plasticity mechanisms. However, the spontaneously post-traumatic recovery of hippocampal-related cognitive and memory functions is very limited. Better under-standing of neurogenesis following TBI may provide additional inter-vention to further enhance neurogenesis for successfully repairing the damaged brain following TBI. Although newborn neurons generated from NSCs are continuously added to the brain throughout our life, they must migrate from their birthplace to their appropriate destina-tion to develop into mature neurons. When we tracked the migration of newly generated neurons in the adult hippocampus after TBI, we found that a large percentage of immature neurons migrate pass their normal stopping site at the inner granular cell layer, and misplace in the outer granular cell layer of the hippocampal dentate gyrus. The aberrant migration of adult-born neurons in the hippocampus occurs 3 days after TBI, and lasts for 10 weeks, resulting in a great number of newly generated neurons misplaced in the outer granular layer in the hippocampus. The newborn neurons at the displaced position will not be able to make correct connections with their appropriate targets, and may even make wrong connections with inappropriate nearby tar-gets in the pre-existing neural network. Abnormal migration can cause several diseases including epilepsy. These results suggest that stimu-lation of endogenous adult neural stem cells following TBI might offer new avenues for cell-based therapy. Additional intervention is required to further enhance successful neurogenesis for repairing the damaged brain.