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PubMed1991

Some cytoarchitectural abnormalities of the entorhinal cortex in schizophrenia.

The cytoarchitecture of the entorhinal cortex was examined in the brains of six patients with a diagnosis of schizophrenia and in 16 controls. All six brains of schizophrenic patients showed abnormalities of the rostral and intermediate portions of the entorhinal cortex. The abnormalities included aberrant invaginations of the surface, disruption of cortical layers, heterotopic displacement of neurons, and paucity of neurons in superficial layers. These changes suggest disturbed development. Because the entorhinal cortex is pivotal for neural systems that mediate corticohippocampal interactions, early disruption of its structure could lead to important neuropsychological changes during development and in adult life and could contribute to the symptomatology of schizophrenia.

Adult↗

PubMed1996

Histological evidence for cholinergic alteration in the hippocampus following entorhinal cortex lesion.

The initial stage of Alzheimer's disease is characterized by neuropathological alteration in the entorhinal cortex. To model one aspect of the neurodegeneration observed and to investigate anatomical changes of the hippocampus associated with unilateral entorhinal cortex lesion, excitotoxin ibotenic acid was used to produce selective unilateral neuronal loss in rat entorhinal cortex. Histological and morphometrical analyses confirmed excitotoxic lesion of the entorhinal cortex after 3 months and showed a decrease of acetylcholineste-rase-stained fibers in the stratum moleculare of the dentate gyrus and the stratum radiatum of the CA3 field. This study demonstrates the importance of the entorhinal cortex in the hippocampal cholinergic function which appears to be important to memory and learning, and raises the possibility that memory deficit in Alzheimer's disease may be associated with partial neuronal loss in the entorhinal cortex.

Acetylcholinesterase↗

PubMed2001

Entorhinal cortex atrophy in epilepsy patients exhibiting normal hippocampal volumes.

OBJECTIVE: To determine whether MRI volumetric measurement of the entorhinal cortex could detect structural damage and lateralize the seizure focus in patients with temporal lobe epilepsy in whom no measurable hippocampal abnormalities were found. BACKGROUND: A reduction in the volume of the entorhinal cortex ipsilateral to the seizure focus in patients with intractable temporal lobe epilepsy and hippocampal atrophy was recently shown. METHODS: MRI volumetric analysis of the entorhinal cortex was performed using a T1-weighted three-dimensional gradient echo sequence in 24 control subjects and 22 patients with temporal lobe epilepsy and normal hippocampal volumes. Thirteen patients underwent surgery, with a mean postoperative follow-up of 36 months. RESULTS: Group analysis (multivariate analysis of variance) showed a reduction in the volume of the entorhinal cortex ipsilateral to the seizure focus in patients with left (p < 0.0001) and right temporal lobe epilepsy (p < 0.0001). Lateralization of the seizure focus could be done in 14 of 22 patients (64%) based on entorhinal cortex volumetry. CONCLUSION: Entorhinal cortex atrophy ipsilateral to the seizure focus supports the presence of structural damage in the mesial temporal lobe in patients with temporal lobe epilepsy and normal hippocampal volumes and emphasizes the participation of the entorhinal cortex in the pathogenesis of this disorder.

Adult↗

PubMed1994

Effect of the infusion of the GABA-A receptor agonist, muscimol, on the role of the entorhinal cortex, amygdala, and hippocampus in memory processes.

Rats were bilaterally implanted with cannulae in the entorhinal cortex, amygdala, and hippocampus; after recovery, they were trained in a step-down inhibitory avoidance task and tested for retention 24 h later. Muscimol (0.03 microgram) or D-amino-5-phosphonovalerate (5.0 micrograms) infused in the entorhinal cortex 20 min prior to training inhibited the amnestic effect of the same dose of muscimol infused into this area 100 min after training. Thus, memory-relevant information must be processed by the entorhinal cortex at the time of training in order that this cortex may play a late post-training role in memory processing. Pretraining intraentorhinal muscimol administration did not affect the amnestic effect of the post-training infusion of muscimol into the amygdala and hippocampus, or the inhibition of memory expression induced by a pretest infusion of CNQX into the amygdala and hippocampus or into the entorhinal cortex. Pretest intraentorhinal muscimol also did not influence the effect of pretest intra-amygdala and intrahippocampal CNQX administration. These data indicate that the cells of the entorhinal cortex that are sensitive to pretraining muscimol are not part of the inputs that lead to post-training processing by the amygdala and hippocampus, or to the intervention of the amygdala, hippocampus, and entorhinal cortex in memory expression. The present findings are compatible with the possibility that, instead, the entorhinal cortex may be an output of the amygdala and hippocampus at the time of memory expression.

2-Amino-5-phosphonovalerate↗

PubMed2000

Cholinergic modulation of synaptic transmission and plasticity in entorhinal cortex and hippocampus of the rat.

Effects of cholinergic agents on synaptic transmission and plasticity were examined in entorhinal cortex and hippocampus. Bath application of carbachol (0.25-0.75 microM) induced transient depression of field potential responses in all cases tested (24/24 in layer III of medial entorhinal cortex slices and 24/24 in CA1 of hippocampal slices; 11.0+/-1.9% and 7.8+/-2.5%, respectively) and long-lasting potentiation in some cases (4/24 in entorhinal cortex and 12/24 in hippocampus; 33.7+/-3.7% and 32.1+/-9.9%, respectively, in successful cases). Carbachol (0.5 microM) induced transient depression, but not long-lasting potentiation, of N-methyl-D-aspartate receptor-mediated responses in entorhinal cortex. At 5 microM, carbachol induced transient depression only (55. 9+/-4.7% in entorhinal cortex and 41.4+/-2.9% in hippocampus), which was blocked by atropine. Paired-pulse facilitation was not altered during carbachol-induced potentiation but enhanced during carbachol-induced depression. These results suggest that the underlying mechanisms of carbachol-induced depression and potentiation are decreased transmitter release and selective enhancement of non-N-methyl-D-aspartate receptor-mediated responses, respectively. Long-term potentiation could be induced in the presence of 10 microM atropine by theta burst stimulation. The magnitude was significantly lower (15.2+/-5.2%, n=9) compared with control (37.2+/-6.1%, n=8) in entorhinal cortex, however. These results demonstrate similar, but not identical, cholinergic modulation of synaptic transmission and plasticity in entorhinal cortex and hippocampus.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed1983

Evidence for a direct projection from the superior temporal gyrus to the entorhinal cortex in the monkey.

During the course of a larger study of the afferent and efferent connections of the entorhinal cortex in the macaque monkey we have found evidence for a hitherto undescribed projection to the entorhinal cortex from the superior temporal gyrus. The evidence is derived principally from experiments in which small volumes of wheat germ agglutinin-conjugated horseradish peroxidase (WGA-HRP) were injected into different parts of the entorhinal cortex, but has been confirmed by 3H-amino acid autoradiography. After WGA-HRP injections into the entorhinal cortex, retrogradely labeled neurons have been seen mainly in layer III, but also to some extent in layer VI, throughout much of the superior temporal gyrus. The projection appears to be topographically organized in the sense that the ventral insular cortex and the adjoining temporal operculum have been found to project to the periamygdaloid cortex and the lateral division of the entorhinal cortex; the convexity of the superior temporal gyrus and the cortex along the dorsal bank of the superior temporal gyrus project further caudally to the medial division of the entorhinal cortex; and the cortex surrounding the fundus of the superior temporal sulcus projects to the perirhinal cortex. Following an injection of 3H-amino acids into the convexity of the superior temporal gyrus, terminal labeling has been seen over layers I and II of the entorhinal cortex and over layer I in the most lateral portion of the presubiculum. While the distribution of retrogradely labeled cells in our WGA-HRP experiments encompasses several cytoarchitectonically distinguishable areas in the superior temporal gyrus, the most heavily labeled field appears to coincide with what Gross and his colleagues have termed the 'superior temporal polysensory area' on the dorsal bank of the superior temporal sulcus.

Afferent Pathways↗

PubMed1992

Parvalbumin and calbindin D-28K in the human entorhinal cortex. An immunohistochemical study.

Research is here reported on the distribution of immunoreactivities of the calcium-binding proteins parvalbumin and calbindin D-28K in the entorhinal cortex of normal human brains. Topographically, parvalbumin immunoreactive neurons were only seen in the lateral portion of the rostral entorhinal cortex, in continuity with the adjacent perirhinal cortex. The intermediate and caudal portions gave positive results along the mediolateral extension of the entorhinal cortex. The laminar distribution of parvalbumin immunoreactive neurons was similar throughout the entorhinal cortex. Heavy immunostaining, largely coincident with cell islands, was observed in cells and fibers in layer II, being densest in the deep half of layer III and more sparsely distributed in layers V and VI. Calbindin D-28K immunoreactivity was found throughout the entorhinal cortex. In contrast to parvalbumin immunoreactivity, calbindin D-28K was present from layer I up to upper layer III, the neurons being most numerous in the cell islands of layer II. These results show that rostromedial portions of the human entorhinal cortex contain calbindin immunoreactivity, but not parvalbumin, while the lateral, intermediate and caudal portions of the entorhinal cortex contain both calcium-binding proteins. As it is known that these two proteins belong to a subset of GABAergic neurons, we suggest that a topographical diversity in some of the cells may be responsible for inhibitory effects in the human entorhinal cortex. This proposed diversity might be relevant to the processing of information that the entorhinal cortex conveys to the dentate gyrus and receives from various components of the hippocampus, the subicular complex and other cortical and subcortical sources.

Calbindins↗

PubMed1998

Perirhinal and postrhinal cortices of the rat: interconnectivity and connections with the entorhinal cortex.

The cortical regions dorsally adjacent to the posterior rhinal sulcus in the rat can be divided into a rostral region, the perirhinal cortex, which shares features of the monkey perirhinal cortex, and a caudal region, the postrhinal cortex, which has connectional attributes similar to the monkey parahippocampal cortex. We examined the connectivity among the rat perirhinal (areas 35 and 36), postrhinal, and entorhinal cortices by placing anterograde and retrograde tracers in all three regions. There is a dorsal-to-ventral cascade of connections in the perirhinal and entorhinal cortices. Dorsal area 36 projects strongly to ventral area 36, and ventral area 36 projects strongly to area 35. The return projections are substantially weaker. The cascade continues with the perirhinal to entorhinal connections. Area 35 is more strongly interconnected with the entorhinal cortex, ventral area 36 somewhat less strongly, and dorsal area 36 projects only weakly to the entorhinal cortex. The postrhinal-to-perirhinal connections also follow this general pattern. The postrhinal cortex is more heavily connected with dorsal area 36 than with ventral area 36 and is more heavily connected with area 36 than with area 35. The rostral portion of the postrhinal cortex has the strongest connections with the perirhinal cortex. Like in the monkey, the perirhinal and postrhinal cortices have different patterns of projections to the entorhinal cortex. The perirhinal cortex is preferentially connected with the rostrolateral portion of the entorhinal cortex. The postrhinal cortex projects to a part of this same region but is also connected to caudal and redial portions of the entorhinal cortex. The perirhinal and postrhinal projections to the entorhinal cortex originate in layers III and V and terminate preferentially in layers II and III.

Animals↗

PubMed1999

Proliferation of microglia and astrocytes in the dentate gyrus following entorhinal cortex lesion: a quantitative bromodeoxyuridine-labelling study.

Entorhinal cortex lesion of adult rats induces glial activation and proliferation in the deafferented dentate molecular layer. Double-labelling immunocytochemistry for the astrocyte-specific antigen glial fibrillary acidic protein or the microglial cell marker Griffonia simplicifolia isolectin B4 with bromodeoxyuridine detection revealed that microglia counts and the proliferation rate in the ipsilateral dentate gyrus reached a maximum in the molecular layer at 3 days post-lesion (dpl) and returned to control levels by 30 dpl. Astrocyte counts in the ipsilateral dentate gyrus peaked at 30 dpl, with maximum proliferation at 7 dpl. At 100 dpl the astrocyte count had reverted to control levels. Glial proliferation was not restricted to the ipsilateral molecular layer but also occurred to some degree in the granule cell layer and the contralateral dentate gyrus. Thus entorhinal cortex lesion induces a rapid microglia reaction and long-lasting astrocyte activation in the deafferented termination zone of the perforant path. We conclude that glial proliferation after entorhinal cortex lesion follows a complex temporal and spatial pattern that coincides with processes of neuronal and axonal reorganization.

Animals↗

PubMed1996

Effects of entorhinal cortex lesion on learning behavior and on hippocampus in the rat.

The initial stage of Alzheimer's disease is characterized by a neuropathological change in the entorhinal cortex. In a previous study it was shown that rats with excitotoxic lesion of entorhinal cortex showed an impaired acquisition of passive and active avoidance responses. In this study a rat with excitotoxic lesion of the entorhinal cortex was tested for 'more operant' behavioral learning (i.e., positive reinforcement operant learning). The hippocampus was also examined histologically as acetylcholinesterase-stained sections, and as synaptophysin immunostained sections and examined biochemically by liquid chromatography. Eight weeks after operation, the bilateral entorhinal cortex lesioned rats showed an impaired acquisition of positive reinforcement operant learning. The lesioned side of unilateral entorhinal cortex lesioned rats showed a decrease of acetylcholinesterase-positive fibers in the CA3, the dentate gyrus, and of synaptophysin-positive substances in the CA3. Biochemical study showed a decreased level of acetylcholine in the CA3, and in the dentate gyrus. The histological and biochemical findings are interpreted as indicating that the entorhinal cortex of the rat provides the major extrinsic synaptic input to the hippocampal formation via the circuit which serves as a relay passage through the dentate gyrus and via direct projections into the hippocampus. Behavioral findings confirmed the importance of the entorhinal cortex in memory acquisition and indicated that rats with a partial neuronal loss in the entorhinal cortex may be a useful model for the memory disturbance of Alzheimer's disease.

Acetylcholine↗

PubMed1998

Density of choline acetyltransferase-immunoreactive terminals in the rat dentate gyrus after entorhinal cortex lesions: a quantitative light microscope study.

Lesion of the entorhinal cortex in the adult rat is a model for Alzheimer's disease and produces a marked increase in acetylcholinesterase (AChE) activity in the outer molecular layer (OML) of the dentate gyrus. This has been attributed to the sprouting of cholinergic axons terminals in response to denervation of the OML. The aim of this study was to investigate the density changes of cholinergic terminals in the OML at the light microscope level by using choline acetyltransferase (ChAT) immunohistochemistry and quantitative analysis. The results showed that between days 10 and 33 after an entorhinal cortex lesion, there was a measurable increase in the density of ChAT-positive boutons in the OML of the ipsilateral dentate gyrus (x1.2-1.6 of contralateral). However, when shrinkage of the ipsilateral OML (x0.5-0.75 of contralateral) was taken into account, the apparent increase in ChAT terminal density was entirely accounted for by shrinkage of the OML. Thus ChAT immunohistochemistry at the light microscope level provides no positive evidence for a proliferation of cholinergic terminals in the entorhinal cortex lesion model. This is in agreement with previous biochemical assays that have shown no change of total ChAT activity in the dentate gyrus after entorhinal cortex lesions.

Acetylcholinesterase↗

PubMed2000

Effects of coupled perirhinal cortex and medial septal area, fimbria-fornix, entorhinal cortex tetrodotoxin inactivations on passive avoidance consolidation in the rat.

In order to ascertain the rat perirhinal cortex (PC) function during early consolidation of a passive avoidance response (PAR), and to ascertain whether there are some functional interactions with the medial septal area (MSA), the fimbria-fornix complex (FF) and the entorhinal cortex (EC), PC-MSA, PC-FF, and PC-EC coupled inactivations were performed immediately after the PAR acquisition session. Anesthetized male adult Wistar rats aged 60 days were treated with stereotaxical bilateral injections of TTX (5 ng in 0.5 microl saline) in the appropriate sites. Retrieval testing was performed 48 h later. It was shown that all three coupled inactivations were followed by significant PAR disruption. It may be concluded that PC is somehow active even during the first mnemonic phase following the acquisition session, thus better defining PC mnemonic involvement chronology. These results may be taken as indicating that during initial consolidation the engram is concurrently processed in more than one septal and parahippocampal site, each of which by itself is not absolutely necessary for the final engram formation.

Analysis of Variance↗

PubMed1999

Entorhinal cortex of aged subjects with Down's syndrome shows severe neuronal loss caused by neurofibrillary pathology.

In Alzheimer's disease (AD), neurofibrillary degeneration of neurons starts in the transentorhinal cortex and spreads in a time-dependent manner to the entorhinal cortex, which provides a major input to the hippocampus--a key structure of the memory system. People with Down's syndrome (DS) develop neurofibrillary changes more than 30 years earlier than those with sporadic AD. To characterize AD-related pathology in the entorhinal cortex in DS, we examined seven subjects with DS of 60-74 years of age who died in the end stage of AD, and four age-matched control subjects. The volume of the entorhinal cortex in brains of subjects with DS was 42% less than that in control cases; however, the total number of neurons free of neurofibrillary changes was reduced in DS by 90%: from 9,619,000 +/- 914,000 (mean +/- standard deviation) to 932,000 +/- 504,000. The presence of 2,488,000 +/- 544,000 neurofibrillary tangles in the entorhinal cortex of people with DS, the prevalence of end-stage tangles, and the significant negative correlation between the total number of intact neurons and the percentage of neurons with neurofibrillary changes indicate that neurofibrillary degeneration is a major cause of neuronal loss in the entorhinal cortex of people with DS. The relatively low amyloid load (7 +/- 1%) and lack of correlation between the amyloid load and the volumetric or neuronal loss suggest that the contribution of beta-amyloid to neuronal loss in the entorhinal cortex is unsubstantial.

Aged↗

PubMed1983

Temporal changes in open-field activity following progressive lesions of entorhinal cortex: evidence for enhanced recovery.

Simultaneous bilateral lesions of the entorhinal cortex typically result in an increase in locomotor activity followed by a decline toward control levels. The present investigation evaluated the effects of "progressive" or "serial" entorhinal lesions on open-field activity. Progressive lesions were made by destroying either the medial or lateral portion of entorhinal cortex bilaterally during one operation and then destroying the remaining portion 11-15 days later. By contrast, serial lesions were made by destroying the entorhinal cortex totally on one side during one operation and then destroying the contralateral side 15 days later. Progressive lesions enhanced the rate and extent of the decline in activity, whereas serial lesions did not. Interoperative testing experience did not appreciably alter the pattern of changes in activity following either type of lesion. The present results indicate that progressive (but not serial) lesions of entorhinal cortex enhance behavioral recovery, and that the degree of recovery following such lesions may be related to the spatial and temporal pattern of sprouting in the hippocampus.

Animals↗

PubMed1997

Entorhinal cortex of the rat: cytoarchitectonic subdivisions and the origin and distribution of cortical efferents.

The origins and terminations of entorhinal cortical projections in the rat were analyzed in detail with retrograde and anterograde tracing techniques. Retrograde fluorescent tracers were injected in different portions of olfactory, medial frontal (infralimbic and prelimbic areas), lateral frontal (motor area), temporal (auditory), parietal (somatosensory), occipital (visual), cingulate, retrosplenial, insular, and perirhinal cortices. Anterograde tracer injections were placed in various parts of the rat entorhinal cortex to demonstrate the laminar and topographical distribution of the cortical projections of the entorhinal cortex. The retrograde experiments showed that each cortical area explored receives projections from a specific set of entorhinal neurons, limited in number and distribution. By far the most extensive entorhinal projection was directed to the perirhinal cortex. This projection, which arises from all layers, originates throughout the entorhinal cortex, although its major origin is from the more lateral and caudal parts of the entorhinal cortex. Projections to the medial frontal cortex and olfactory structures originate largely in layers II and III of much of the intermediate and medial portions of the entorhinal cortex, although a modest component arises from neurons in layer V of the more caudal parts of the entorhinal cortex. Neurons in layer V of an extremely laterally located strip of entorhinal cortex, positioned along the rhinal fissure, give rise to the projections to lateral frontal (motor), parietal (somatosensory), temporal (auditory), occipital (visual), anterior insular, and cingulate cortices. Neurons in layer V of the most caudal part of the entorhinal cortex originate projections to the retrosplenial cortex. The anterograde experiments confirmed these findings and showed that in general, the terminal fields of the entorhinal-cortical projections were densest in layers I, II, and III, although particularly in the more densely innervated areas, labeling in layer V was also present. Comparably distributed, but much weaker projections reach the contralateral hemisphere. Our results show that in the rat, hippocampal output can reach widespread portions of the neocortex through a relay in a very restricted part of the entorhinal cortex. However, most of the hippocampal-cortical connections will be mediated by way of entorhinal-perirhinal-cortical connections. We conclude that, in contrast to previous notions, the overall organization of the hippocampal-cortical connectivity in the rat is largely comparable to that in the monkey.

Amygdala↗

PubMed1996

Projections from the nucleus reuniens thalami to the entorhinal cortex, hippocampal field CA1, and the subiculum in the rat arise from different populations of neurons.

The entorhinal cortex, CA1, and the subiculum receive a major input from the thalamic midline nucleus reuniens. At present, it is not known whether reuniens projections to these intimately interconnected regions are collateralized or arise from different cell populations. We employed the multiple fluorescent retrograde tracing technique with Fast Blue, Diamidino Yellow, and Fluoro-Gold to examine the possible collateralization of reuniens projections to the entorhinal cortex, CA1, and the subiculum. In addition, we studied the extent of collateralization within each target area. The results indicate that different, yet morphologically indistinguishable, populations of reuniens cells selectively innervate the entorhinal cortex, CA1, or subiculum. Within each of these areas, reuniens fibers display a locally restricted collateralization instead of distributing collaterals throughout the entire target structure. The rostal two-thirds of the nucleus reuniens is the major source of ipsilateral projections to CA1, subiculum, and entorhinal cortex. The perireuniens nucleus selectively projects to the perirhinal cortex. Reuniens projections to CA1 and medial entorhinal cortex originate in the dorsolateral part and throughout the medial one-half of the nucleus, respectively. For these two projections, no topography could be established. However, subicular afferents are topographically organized such that a dorsal-to-ventral gradient in the nucleus reuniens corresponds to a dorsal-to-ventral gradient along the subicular axis. Lateral entorhinal afferents display a subtle topography such that a lateral-to-medial shift of terminal fields in the lateral entorhinal cortex corresponds to a lateral-to-medial shift of projection neurons in the ventral nucleus reuniens.

Animals↗

PubMed1993

Regional and laminar organization of projections from the presubiculum and parasubiculum to the entorhinal cortex: an anterograde tracing study in the rat.

The regional and laminar organization of the projections from the presubiculum and the parasubiculum to the entorhinal cortex was analyzed in the rat with the anterograde tracer Phaseolus vulgaris-leucoagglutinin (PHA-L). The projections from the presubiculum were bilateral and confined to layers III and I of the medial entorhinal area (MEA). Both the ispi- and the contralateral projections showed similar distributions and were almost of equal density. Projections to layer III of the entorhinal cortex arose predominantly from superficial layers of the presubiculum, whereas the fibers that reach layer I of the entorhinal cortex appear to originate preferentially from the deep layers of the presubiculum. These fibers also appeared to innervate weakly layer II of MEA. The parasubiculum distributed projections not only to MEA but also to the lateral entorhinal area (LEA), innervating layer II selectively. The innervation of LEA was quite dense and extensive. Very weak projections from the parasubiculum to the contralateral entorhinal cortex were observed in this study. The position of the terminal plexus in the entorhinal cortex was determined by the point of origin along both the dorsoventral and transverse or proximodistal axes of the presubiculum and parasubiculum. Projections from the presubiculum and parasubiculum entered the entorhinal cortex at the level of the injection, or slightly ventral to it, and the main terminal field was always present ventrally to the injection site. The dorsoventral axis of origin thus corresponded to a similarly oriented axis of termination in the entorhinal cortex. The distribution in relation to the origin along the transverse axis was more complex, and differences between the presubiculum and parasubiculum were present. The proximal presubiculum, i.e., the part closest to the subiculum, projected to the most lateral part of MEA and the central part of the presubiculum sent fibers to the most medial part of MEA. The distal part of the presubiculum, i.e., the part that borders the parasubiculum, projected to the central part of MEA. Projections from the portion of the parasubiculum directly adjacent to the presubiculum, the so-called proximal parasubiculum, reached medial parts of MEA, and those originating in the central part distributed preferentially to lateral parts of MEA and adjacent medial parts of LEA. The distal part of the parasubiculum that borders the entorhinal cortex projected mainly to almost the full mediolateral extent of LEA.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2000

Usefulness of MRI measures of entorhinal cortex versus hippocampus in AD.

OBJECTIVE: MRI-based measurements of hippocampal atrophy are a sensitive indicator of the early pathologic degeneration of the medial temporal lobe in AD. However, AD pathology appears first in the transentorhinal/entorhinal cortex, not the hippocampus. The authors tested the hypothesis that MRI-based measurements of the entorhinal cortex are more sensitive than measurements of hippocampal volume in discriminating among three clinical groups; controls, patients with a mild cognitive impairment (MCI), and patients with mild probable AD. METHODS: The authors studied 30 controls, 30 patients with MCI, and 30 patients with AD who were matched among clinical groups on age, gender, and education. All underwent a standardized MRI protocol from which the authors made measurements of hippocampal volume, entorhinal cortex volume, and the cumulative length of the medial border of the entorhinal cortex. RESULTS: Pairwise intergroup differences (p < 0.01) were found for all MRI measurements with the exception of the cumulative length of the entorhinal cortex, which did not differentiate controls from MCI patients. Whereas the hippocampal and entorhinal cortex volume measurements provided slightly better intergroup discrimination than the entorhinal distance measurement, overall differences in discriminating ability among the three MRI measurements were minor. CONCLUSIONS: Despite the theoretical rationale for the superiority of entorhinal measurements in early AD, the authors found MRI measurements of the hippocampus and entorhinal cortex were approximately equivalent at intergroup discrimination. Measurements of the hippocampus may be preferable because MRI depiction of the boundaries of the entorhinal cortex can be obscured by anatomic ambiguity, image artifact, or both.

Aged↗