Episodic memories reflect a bound representation of multimodal features that can be reinstated with varying precision. Yet little is known about how brain networks involved in memory, including the hippocampus and posterior-medial (PM) and anterior-temporal (AT) systems, interact to support the quality and content of recollection. Participants learned color, spatial, and emotion associations of objects, later reconstructing the visual features using a continuous color spectrum and 360-degree panorama scenes. Behaviorally, dependencies in memory were observed for the gist but not precision of event associations. Supporting this integration, hippocampus, AT, and PM regions showed increased connectivity and reduced modularity during retrieval compared to encoding. These inter-network connections tracked a multidimensional, objective measure of memory quality. Moreover, distinct patterns of connectivity tracked item color and spatial memory precision. These findings demonstrate how hippocampal-cortical connections reconfigure during episodic retrieval, and how such dynamic interactions might flexibly support the multidimensional quality of remembered events.
Data and code have been made available via GitHub: https://github.com/memobc/paper-orbitfmri
A functional neuroimaging study of item and spatial context memory precisionGitHub, memobc/paper-orbitfmri.
Visual long-term memory has the same limit on fidelity as visual working memorybradylab.ucsd.edu, stimuli.
Recognizing Scene Viewpoint using Panoramic Place Representationpeople.csail.mit.edu/jxiao, SUN360.
The International Affective Digitized Sounds (2nd Edition; IADS-2)csea.phhp.ufl.edu, IADS.
- Maureen Ritchey
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Human subjects: Informed consent was obtained from all participants prior to the experiment. Procedures were approved by the Boston College Institutional Review Board (17.026).
- Muireann Irish, University of Sydney, Australia
© 2019, Cooper & Ritchey
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
Infantile neuroaxonal dystrophy (INAD) is caused by recessive variants in PLA2G6 and is a lethal pediatric neurodegenerative disorder. Loss of the Drosophila homolog of PLA2G6, leads to ceramide accumulation, lysosome expansion, and mitochondrial defects. Here, we report that retromer function, ceramide metabolism, the endolysosomal pathway, and mitochondrial morphology are affected in INAD patient-derived neurons. We show that in INAD mouse models, the same features are affected in Purkinje cells, arguing that the neuropathological mechanisms are evolutionary conserved and that these features can be used as biomarkers. We tested 20 drugs that target these pathways and found that Ambroxol, Desipramine, Azoramide, and Genistein alleviate neurodegenerative phenotypes in INAD flies and INAD patient-derived neural progenitor cells. We also develop an AAV-based gene therapy approach that delays neurodegeneration and prolongs lifespan in an INAD mouse model.
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