The entorhinal cortex is a region of the brain, located on the underside of the cortex near the hippocampus (see Amaral, 1999& Hafting, Fyhn, Molden, Moser, & Moser, 2005). The following figure presents the left entorhinal cortex in red, as viewed from below the cortex.
The entorhinal cortex is the main conduit between the hippocampus and the neocortex. In particular, the entorhinal cortex supplies the hippocampus with information from multiple senses. In addition, the entorhinal cortex also translates information from the hippocampus to the neocortex. Glutamate is the main neurotransmitter that mediates the transmission of information between the entorhinal cortex and hippocampus. Hence, the entorhinal cortex is involved in the consolidation of memories, particularly during periods of sleep.
Apart from this role as a conduit, the entorhinal cortex retains sensory experiences while individuals determine whether the stimulus conditions are novel or familiar. That is, the hippocampus determines whether the sensory experience retained in the entorhinal cortex has already been represented in memory previously.
The properties of the entorhinal cortex differ across the various areas of this region. For example, neurons in the medial entorhinal cortex respond only to specific locations, called spatial selectivity, usually arranged in hexagonal patterns. The size of these fields increases from the dorso-lateral to the ventro-medial portions of the medial entorhinal cortex. In contrast, neurons in the lateral entorhinal cortex do not seem to show this spatial selectivity (see Hargreaves Rao Lee Knierim 2005).
In Alzheimer's Disease, neuritic amyloid plaques are distributed throughout the cortex (see Braak & Braak, 1991). A progressive and incessant imbalance between the production and elimination of amino acid peptide fragments, called beta-amyloid, consolidate to form these amyloid plaques. These plaques first appear in the neocortex, followed by the entorhinal cortex, insular cortex, and hippocampus (Thal, R?b, Orantes, & Braak, 2002).
Furthermore, in Alzheimer's Disease, neurofibrillary tangles are dispersed throughout the brain. Neurofibrillary tangles appear within neurons and comprise hyper-phosphorylated tau protein-a protein that is needed to stabilize the microtubule system that underpins intracellular transport. Extra phosphate groups combine with the tau protein. In response, this tau protein forms pairs of helical filaments called neurofibrillary tangles-a process that is expedited by beta-amyloid deposits (e.g., Selkoe, 2000). These tangles first form in the trans-entorhinal region before extending to the entorhinal cortex, hippocampus, and ultimately the neocortex (Braak & Braak, 1991).
Atrophy of the entorhinal cortex is not only implicated in Alzheimer's Disease, but has also been demonstrated in mild cognitive impairment-which is often a precursor to Alzheimer's Disease. For example, MRI studies have uncovered atrophy in the entorhinal cortex and hippocampus in individuals with mild cognitive impairment (see deToledo-Morrell et al., 2004) or Alzheimer's Disease (see Teipel et al., 2006). The level of atrophy does not distinguish mild from moderate Alzheimer's Disease (see Teipel et al., 2006).
These reductions in the entorhinal cortex might explain some of the deficits in memory consolidation, short term retention, and other cognitive functions in Alzheimer's Disease and mild cognitive impairment. Furthermore, because the entorhinal cortex is involved in comparing sensory events to previous representations, atrophy in this structure could explain some misconceptions and overgeneralizations of negative events (Prasad, Patel, Muddasani Sweeney, & Keshavan, 2004).
Preliminary research indicates the entorhinal cortex might be implicated in clinical depression. Bell-McGinty, Butters, Meltzer, Greer, Reynolds III, and Becker (2002), for example, showed the right region of the entorhinal cortex and hippocampus combined is smaller in elderly individuals with depression.
Nevertheless, this study does present some key limitations. First, the study did not distinguish the entorhinal cortex from the hippocampus, and previous research has already established that hippocampal volume does depend on depression. Second, this study used voxel-based morphemetric methods to gauge the volume of these regions. Voxel-based morphemetric differences can represent changes in voxel intensity rather than atrophy.
In the context of schizophrenia, atrophy seems to begin in the entorhinal cortex before extending to the hippocampus and amygdala (Laakso, Frisoni, Kononen, Mikkonen, Beltramello, & Geroldi, 2000).
Under continued stress, neuronal damage has been discovered in the entorhinal cortex. That is, stress enhances glutamatergic transmission, which culminates in the death of neurons with postsynaptic glutamate receptors-which are common in the entorhinal cortex and hippocampus.
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Last Update: 6/15/2016