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Fuqiang Gao
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Journal Articles
Publisher: Journals Gateway
Journal of Cognitive Neuroscience (2011) 23 (12): 3804–3816.
Published: 01 December 2011
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Medial-temporal, parietal, and pFC regions have been implicated in recollection and familiarity, but existing evidence from neuroimaging and patient studies is limited and conflicting regarding the role of specific regions within pFC in these memory processes. We report a study of 20 patients who had undergone resection of right frontal lobe tumors and 20 matched healthy control participants. The location and extent of lesions were traced on the patients' scans. A process dissociation procedure was employed to yield estimates of the contributions of recollection and familiarity in verbal recognition performance. Group comparisons revealed deficits in recollection but not familiarity in the patient group relative to their healthy counterparts. We found a positive relationship between estimates of familiarity and lesion sizes in the right inferior pFC (BA 11, 47) which was significant upon bootstrap resampling. These results are discussed in terms of prior work linking this area to an overextended sense of familiarity.
Journal Articles
Publisher: Journals Gateway
Journal of Cognitive Neuroscience (2008) 20 (8): 1490–1506.
Published: 01 August 2008
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The issue of whether the hippocampus and related structures in the medial-temporal lobe (MTL) play a temporary or permanent role in autobiographical episodic memory remains unresolved. One long-standing belief is that autobiographical memory (AM), like semantic memory, is initially dependent on the MTL but ultimately can be retained and recovered independently of it. However, evidence that hippocampal amnesia results in severe loss of episodic memory for a lifetime of personally experienced events suggests otherwise. To test the opposing views, we conducted detailed investigations of autobiographical episodic memory in people with amnesia resulting from MTL lesions of varying extent. By combining precise quantification of MTL and neocortical volumes with sensitive measures of recollection of one's personal past, we show that the severity of episodic, but not semantic, AM loss is best accounted for by the degree of hippocampal damage and less likely related to additional neocortical compromise.
Journal Articles
Publisher: Journals Gateway
Journal of Cognitive Neuroscience (2005) 17 (3): 446–462.
Published: 01 March 2005
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Recent research suggests that the hippocampus is not needed for the maintenance and recovery of extensively used environments learned long ago. Instead, a network of neo-cortical regions differentially supports memory for location-navigation knowledge and visual appearance of well-known places. In this study, we present a patient, S. B., who was diagnosed with probable Alzheimer's disease long after retiring from his 40 years as a taxi driver in downtown Toronto, a place that he has visited rarely, if ever, in the last decade. His performance was compared to that of two other retired taxi drivers, L. R., who developed encephalitis after retirement, and I. L., who is without neurological illness, and a group of eight healthy control participants who were never taxi drivers but all of whom worked or lived in downtown Toronto until at least 10 years ago. Despite S. B.'s widespread atrophy, which has affected mainly his hippocampus and part of his occipitotemporal cortex, he performed at least as well as all other participants on remote memory tests of spatial location and mental navigation between well-known Toronto landmarks. Unlike the comparison populations, however, he was unable to discriminate between the appearances of landmarks that he had visited frequently in his many years as a taxi driver from unknown buildings. This profound deficit extended to famous world landmarks but not to famous faces and does not appear to be semantic in nature. These findings add further support to the claim that the hippocampus is not necessary for mental navigation of old environments and suggest that expertise is not sufficient to protect against landmark agnosia.