Imaging the Networks of Encoding, Consolidation, and Retrieval

Author(s):  
Andrew C. Papanicolaou ◽  
Nicole Shay ◽  
Christen M. Holder

In this chapter, the authors examine the contributions of the functional neuroimaging literature to the specification of the neuronal networks of the mnemonic operations of encoding, consolidation, and retrieval. Although the most basic expectation regarding the involvement of parts of the medial temporal lobes, such as the hippocampus, in these operations was not consistently supported by the results of the neuroimaging studies reviewed, other expectations, such as the material-specific lateralization of activation were adequately supported. The several reasons that account for the limited contributions of neuroimaging to the neurophysiology of memory thus far, ranging from constraints imposed by the nature of the mnemonic operations (e.g., the fact that encoding and retrieval occur in tandem) to practical ones (e.g., difficulties in studying spontaneous retrieval), are outlined.

2001 ◽  
Vol 356 (1413) ◽  
pp. 1395-1408 ◽  
Author(s):  
Andrew R. Mayes ◽  
Neil Roberts

Theories of episodic memory need to specify the encoding (representing), storage, and retrieval processes that underlie this form of memory and indicate the brain regions that mediate these processes and how they do so. Representation and re–representation (retrieval) of the spatiotemporally linked series of scenes, which constitute an episode, are probably mediated primarily by those parts of the posterior neocortex that process perceptual and semantic information. However, some role of the frontal neocortex and medial temporal lobes in representing aspects of context and high–level visual object information at encoding and retrieval cannot currently be excluded. Nevertheless, it is widely believed that the frontal neocortex is mainly involved in coordinating episodic encoding and retrieval and that the medial temporal lobes store aspects of episodic information. Establishing where storage is located is very difficult and disagreement remains about the role of the posterior neocortex in episodic memory storage. One view is that this region stores all aspects of episodic memory ab initio for as long as memory lasts. This is compatible with evidence that the amygdala, basal forebrain, and midbrain modulate neocortical storage. Another view is that the posterior neocortex only gradually develops the ability to store some aspects of episodic information as a function of rehearsal over time and that this information is initially stored by the medial temporal lobes. A third view is that the posterior neocortex never stores these aspects of episodic information because the medial temporal lobes store them for as long as memory lasts in an increasingly redundant fashion. The last two views both postulate that the medial temporal lobes initially store contextual markers that serve to cohere featural information stored in the neocortex. Lesion and functional neuroimaging evidence still does not clearly distinguish between these views. Whether the feeling that an episodic memory is familiar depends on retrieving an association between a retrieved episode and this feeling, or by an attribution triggered by a priming process, is unclear. Evidence about whether the hippocampus and medial temporal lobe cortices play different roles in episodic memory is conflicting. Identifying similarities and differences between episodic memory and both semantic memory and priming will require careful componential analysis of episodic memory.


eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Maureen Ritchey ◽  
Maria E Montchal ◽  
Andrew P Yonelinas ◽  
Charan Ranganath

The medial temporal lobes play an important role in episodic memory, but over time, hippocampal contributions to retrieval may be diminished. However, it is unclear whether such changes are related to the ability to retrieve contextual information, and whether they are common across all medial temporal regions. Here, we used functional neuroimaging to compare neural responses during immediate and delayed recognition. Results showed that recollection-related activity in the posterior hippocampus declined after a 1-day delay. In contrast, activity was relatively stable in the anterior hippocampus and in neocortical areas. Multi-voxel pattern similarity analyses also revealed that anterior hippocampal patterns contained information about context during item recognition, and after a delay, context coding in this region was related to successful retention of context information. Together, these findings suggest that the anterior and posterior hippocampus have different contributions to memory over time and that neurobiological models of memory must account for these differences.


Hippocampus ◽  
2021 ◽  
Author(s):  
Thackery I. Brown ◽  
Qiliang He ◽  
Irem Aselcioglu ◽  
Chantal E. Stern

2021 ◽  
pp. 1-11
Author(s):  
Adam S. Bernstein ◽  
Steven Z. Rapcsak ◽  
Michael Hornberger ◽  
Manojkumar Saranathan ◽  

Background: Increasing evidence suggests that thalamic nuclei may atrophy in Alzheimer’s disease (AD). We hypothesized that there will be significant atrophy of limbic thalamic nuclei associated with declining memory and cognition across the AD continuum. Objective: The objective of this work was to characterize volume differences in thalamic nuclei in subjects with early and late mild cognitive impairment (MCI) as well as AD when compared to healthy control (HC) subjects using a novel MRI-based thalamic segmentation technique (THOMAS). Methods: MPRAGE data from the ADNI database were used in this study (n = 540). Healthy control (n = 125), early MCI (n = 212), late MCI (n = 114), and AD subjects (n = 89) were selected, and their MRI data were parcellated to determine the volumes of 11 thalamic nuclei for each subject. Volumes across the different clinical subgroups were compared using ANCOVA. Results: There were significant differences in thalamic nuclei volumes between HC, late MCI, and AD subjects. The anteroventral, mediodorsal, pulvinar, medial geniculate, and centromedian nuclei were significantly smaller in subjects with late MCI and AD when compared to HC subjects. Furthermore, the mediodorsal, pulvinar, and medial geniculate nuclei were significantly smaller in early MCI when compared to HC subjects. Conclusion: This work highlights nucleus specific atrophy within the thalamus in subjects with early and late MCI and AD. This is consistent with the hypothesis that memory and cognitive changes in AD are mediated by damage to a large-scale integrated neural network that extends beyond the medial temporal lobes.


2017 ◽  
Vol 27 ◽  
pp. S538-S539
Author(s):  
T.J.M. Roelofs ◽  
J.P.H. Verharen ◽  
G.A.F. Van Tilborg ◽  
L. Boekhoudt ◽  
A. Van der Toorn ◽  
...  

Author(s):  
Briana S. Last ◽  
Batool Rizvi ◽  
Adam M. Brickman

Structural magnetic resonance imaging (MRI) is a powerful tool to visualize and quantitate morphological and pathological features of the aging brain. Most work that has used structural MRI to study Alzheimer’s disease (AD) focused on the spatial distribution of atrophic changes associated with disease. These studies consistently show focal atrophy beginning in medial temporal lobes in early and presymptomatic stages of AD before spreading globally throughout the cortical mantle. Normal cognitive aging—aging in the absence of major neurodegenerative disease—on the other hand follows and anterior-to-posterior gradient of atrophic change. In addition to atrophic changes, conventional structural MRI can be used to appreciate markers of small and large vessel cerebrovascular disease, including white matter hyperintensities (WMHs), cerebral microbleeds, and infarction. Studies that have examined cerebrovascular changes associated with AD also show a consistent relationship with risk and severity of clinical AD, particularly with regard to lobar microbleeds and posterior WMH. It is unclear whether cerebrovascular changes play an independent role in the clinical expression of AD or whether it is more mechanistically related, reflecting a core feature of the disease. This chapter reviews recent work on regional atrophy in AD and normal aging, as well as work on small and large cerebrovascular disease in AD.


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