Hemispheric differences in hippocampal volume predict verbal and spatial memory performance in patients with Alzheimer's disease

Department of Neurological Sciences, Rush University, Chicago, Illinois, USA.
Hippocampus (Impact Factor: 4.16). 01/2000; 10(2):136-42. DOI: 10.1002/(SICI)1098-1063(2000)10:2<136::AID-HIPO2>3.0.CO;2-J
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Atrophy of the hippocampal formation, a region important for the acquisition of new declarative knowledge, has been well-documented in Alzheimer's disease (AD), although the relation of such atrophy to the extent of memory dysfunction in these patients has been less clear. In the present study, 18 patients with a clinical diagnosis of probable AD were studied with a high-resolution, quantitative magnetic resonance imaging (MRI) protocol, as well as the verbal and spatial versions of the Buschke controlled learning task. The volumes of the hippocampal formation and, as a control for generalized atrophy, parahippocampal gyrus and temporal neocortex were computed from gapless coronal slices taken perpendicular to the long axis of the hippocampus. To correct for individual differences in brain size, volumes of regions of interest were divided by total intracranial volume. Separate stepwise regression analyses (with age, right and left hippocampal, parahippocampal gyrus, and temporal lobe volumes as the independent variables) showed that left hippocampal volume was the best predictor of free recall and delayed free recall of verbal information (P = 0.0042 and P < 0.0001, respectively). Recall and delayed recall of the spatial location of verbal items were best predicted by right hippocampal volume (P = 0.0054 and P = 0.0118, respectively). Memory scores did not correlate either with parahippocampal gyrus or temporal lobe volume. Furthermore, the relation between hippocampal volume and memory function observed in cases with AD did not hold for healthy aged control subjects.

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Available from: Bradford Dickerson, Jan 21, 2014
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    • "Episodic memory dysfunction represents a hallmark feature of this patient group, in light of the characteristic medial temporal lobe degeneration evident from an early stage in the pathological process (Braak & Braak, 1991). An amnestic profile predominates whereby AD patients exhibit anterograde episodic memory difficulties concerning the encoding and retrieval of recent experiences, irrespective of task modality (McKhann et al., 2011; de Toledo-Morrell et al., 2000). Retrograde memory impairments are also prominent, manifesting in pronounced autobiographical memory dysfunction (Barnabe, Whitehead, Pilon, Arsenault-Lapierre, & Chertkow, 2012; Irish, Hornberger, et al., 2011, Irish, Lawlor, O'Mara, & Coen, 2011), which is significantly associated with the degree of medial and lateral temporal lobe atrophy (Gilboa et al., 2005). "
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    ABSTRACT: Episodic memory dysfunction represents one of the most prominent and characteristic clinical features of patients with Alzheimer's disease (AD), attributable to the degeneration of medial temporal and posterior parietal regions of the brain. Recent studies have demonstrated marked impairments in the ability to envisage personally relevant events in the future in AD. It remains unclear, however, whether AD patients can imagine fictitious scenes free from temporal constraints, a process that is proposed to rely fundamentally upon the integrity of the hippocampus. The objective of the present study was to investigate the capacity for atemporal scene construction, and its associated neural substrates, in AD. Fourteen AD patients were tested on the scene construction task and their performance was contrasted with 14 age- and education-matched healthy older Control participants. Scene construction performance was strikingly compromised in the AD group, with significant impairments evident for provision of contextual details, spatial coherence, and the overall richness of the imagined experience. Voxel-based morphometry analyses based on structural MRI revealed significant associations between scene construction capacity and atrophy in posterior parietal and lateral temporal brain structures in AD. In contrast, scene construction performance in Controls was related to integrity of frontal, parietal, and medial temporal structures, including the parahippocampal gyrus and posterior hippocampus. The posterior cingulate cortex (PCC) emerged as the common region implicated for scene construction performance across participant groups. Our study highlights the importance of regions specialised for spatial and contextual processing for the construction of atemporal scenes. Damage to these regions in AD compromises the ability to construct novel scenes, leading to the recapitulation of content from previously experienced events.
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    • "The theoretical prominence of the MTLs, in particular the hippocampus, in episodic memory is supported by studies of patients with probable AD, in which episodic memory decline is the hallmark feature [Nestor et al., 2006; McKhann et al., 2011]. Unsurprisingly, AD patients show episodic memory deficits extending across standard neuropsychological tests of visual and verbal recall [de Toledo-Morrell et al., 2000], as well as the retrieval of personally relevant episodic autobiographical memories [Piolino et al., 2003; Irish et al., 2011b]. This loss of episodic memory in AD has been interpreted in relation to the characteristic pattern of atrophy beginning in the entorhinal cortex and progressing across the hippocampus to the neocortex [Braak and Braak, 1991], as well as the involvement of more posterior structures including the posterior cingulate cortex [Nestor et al., 2006]. "
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    No preview · Article · Apr 2014 · Human Brain Mapping
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    • "Recent studies point to the preferential accumulation of amyloid deposits in specific nodes of the core ABM network in AD, most notably the posterior cingulate cortex and the anteromedial prefrontal cortex (Buckner et al., 2008). Clinically, AD patients typically present with an amnestic profile in which anterograde episodic memory difficulties concerning the encoding and retrieval of recent events are prominent (de Toledo-Morrell et al., 2000; McKhann et al., 2011). This disruption to episodic memory emerges as a consequence of the neuropathological process (neurofibrillary tangles and amyloid deposition), which affects the entorhinal cortex and hippocampus of the medial temporal lobes, and spreads to the neocortex (Ewers et al., 2011; Sperling et al., 2011). "
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