MRI-derived entorhinal and hippocampal atrophy in incipient and very mild Alzheimer’s disease ☆ ☆This research was supported by grants P01 AG09466 and P30 AG10161 from the National Institute on Aging, National Institutes of Health.

Dickerson, Brad C.; Goncharova, Irina I.; Sullivan, Michael P.; Forchetti, Concetta; Wilson, Robert S.; Bennett, David A.; Beckett, Laurel A.; deToledo-Morrell, Leyla

doi:10.1016/s0197-4580(01)00271-8

Cited by 426 publications

(111 citation statements)

References 45 publications

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“…A previous report from our laboratory showed that the right entorhinal cortex was somewhat larger than the left in participants with subjective cognitive complaints and in elderly controls (20). In the present study, although the same asymmetry was evident in controls, it was not significant in participants with frank MCI.…”

Section: Discussioncontrasting

confidence: 65%

Hippocampal disconnection contributes to memory dysfunction in individuals at risk for Alzheimer’s disease

Stoub¹,

deToledo-Morrell²,

Stebbins³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

162

128

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The concept of amnestic mild cognitive impairment (MCI) describes older people who show a decline predominantly in memory function, but who do not meet criteria for dementia. Because such individuals are at high risk for developing Alzheimer's disease, they are of great interest for understanding the prodromal stages of the disease process. The mechanism underlying memory dysfunction in people with MCI is not fully understood. The present study uses quantitative, high-resolution structural MRI techniques to investigate, in vivo, the anatomical substrate of memory dysfunction associated with MCI. Changes in brain structures were assessed with two imaging techniques: (i) whole-brain, voxelbased morphometry to determine regions of reduced white matter volume and (ii) sensitive volumetric segmentation of the entorhinal cortex and hippocampus, gray matter regions that are critically important for memory function. In participants with amnestic MCI, compared with age-matched controls, results showed a significant decrease in white matter volume in the region of the parahippocampal gyrus that includes the perforant path. There was also significant atrophy in both the entorhinal cortex and the hippocampus. Regression models demonstrated that both hippocampal volume and parahippocampal white matter volume were significant predictors of declarative memory performance. These results suggest that, in addition to hippocampal atrophy, disruption of parahippocampal white matter fibers contributes to memory decline in elderly individuals with MCI by partially disconnecting the hippocampus from incoming sensory information.entorhinal cortex ͉ imaging ͉ parahippocampal gyrus ͉ perforant path ͉ voxel-based morphometry O ne of the first clinically recognized symptoms of Alzheimer's disease (AD) is diminished performance on tests assessing declarative memory function. The brain regions critically important for this type of memory are the hippocampus and related mesial temporal lobe structures (1-3). Previous histopathological findings (4-10) indicate that the entorhinal cortex and hippocampus are pathologically involved very early in patients with AD and in individuals with mild cognitive impairment (MCI) who are at high risk for developing AD (11,12). Specifically, two of these studies (7, 9) found a loss of entorhinal cortex layer II neurons in patients with AD and in those with MCI, compared with controls. These neurons receive multimodal sensory input from primary sensory and association cortices and project this information to the hippocampus via the perforant path, a white matter tract located in the anterior medial portion of the parahippocampal gyrus (13-15). Therefore, the loss of layer II neurons in the entorhinal cortex could essentially cause a disconnection of information flow to the hippocampus (10). In addition, damage to the white matter of the parahippocampal gyrus could disrupt afferent connections to the entorhinal cortex and ultimately disconnect multimodal sensory input to the hippocampus, information vital to th...

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Section: Discussioncontrasting

confidence: 65%

Hippocampal disconnection contributes to memory dysfunction in individuals at risk for Alzheimer’s disease

Stoub¹,

deToledo-Morrell²,

Stebbins³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

162

128

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“…One big leap in this field is imaging of the amyloid burden in CIS or MS patients. Molecular neuroimaging techniques such as PET have been used for the in vivo assessment of molecular processes at their sites of action, permitting the detection of subtle pathophysiological changes in the brain at asymptomatic stages when there is no evidence of anatomic changes on CT or MR imaging [24,25,26,27]. To detect ongoing demyelination and remyelination in MS, PET with ligands for myelin may be more specific.…”

Section: Importance Of Early Prediction Of Msmentioning

confidence: 99%

Role of Amyloid from a Multiple Sclerosis Perspective: A Literature Review

Chandra¹

2015

Neuroimmunomodulation

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The traditional concept of multiple sclerosis (MS), that it is primarily a white matter inflammatory disease, has changed a great deal. Thanks to the recent development witnessed in MS research, a whole new idea has emerged that MS is a neurodegenerative disease, and neurodegeneration occurs rather earlier in the pathological process. This has also led to the foundation of the hypothesis that two fundamentally different diseases, Alzheimer's disease (AD) and MS, may share a common mechanism of neurodegeneration. Conventionally, amyloid is thought to be a consequence of protein misfolding and aggregation and is most notorious for its association with debilitating and chronic human diseases. Amyloid is implicated to be related with the deterioration and progression of AD. The finding of amyloid precursor protein expression in axons around the plaque in MS, as well as the correlation of amyloid-β (Aβ) with different stages of MS, has clearly indicated that amyloid plays some kind of key role in MS disease pathogenesis. Excitingly, a paradoxical phenomenon of Aβ has also been observed in several studies recently. It has been shown that amyloid might actually be helping in ameliorating the inflammatory effect in diseases like AD and MS. Amyloid imaging allows earlier diagnosis of MS by taking advantage of the relation of amyloid with MS. This will have a big impact on patient diagnosis and management. In this review I have included the findings of research studies dating from several years back to the most recent ones. Through this review I have tried to show the critical role of amyloid in MS and the importance of investigating through PET imaging.

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“…Volumetric assessment, comparing the volumes of various brain structures across subjects from the three different groups, is the most popular and direct way. Researchers in prior studies have focused primarily on medial temporal regions, demonstrating atrophy of hippocampus and entorhinal cortex in individuals with MCI or AD compared to those measured in controls [Atiya et al, 2003; Bell-McGinty et al, 2002; Dickerson et al, 2001; Frisoni and Caroli, 2007; Jack et al, 1999; Killiany et al, 2002] and ventricle enlargement in both MCI and AD [Chetelat and Baron, 2003; McKhann et al, 1984; Ridha et al, 2008]. Volumes of other subcortical nuclei such as amygdala, putamen, caudate, and thalamus have also been reported to be affected in MCI and AD [Convit et al, 2000; de Jong et al, 2008; Madsen et al, 2010; Visser et al, 1999; Whitehouse et al, 1982].…”

Section: Introductionmentioning

confidence: 99%

Shape abnormalities of subcortical and ventricular structures in mild cognitive impairment and Alzheimer's disease: Detecting, quantifying, and predicting

Tang

Holland

Dale

et al. 2014

Human Brain Mapping

131

165

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This article assesses the feasibility of using shape information to detect and quantify the subcortical and ventricular structural changes in mild cognitive impairment (MCI) and Alzheimer’s disease (AD) patients. We first demonstrate structural shape abnormalities in MCI and AD as compared with healthy controls (HC). Exploring the development to AD, we then divide the MCI participants into two subgroups based on longitudinal clinical information: (1) MCI patients who remained stable; (2) MCI patients who converted to AD over time. We focus on seven structures (amygdala, hippocampus, thalamus, caudate, putamen, globus pallidus, and lateral ventricles) in 754 MR scans (210 HC, 369 MCI of which 151 converted to AD over time, and 175 AD). The hippocampus and amygdala were further subsegmented based on high field 0.8 mm isotropic 7.0T scans for finer exploration. For MCI and AD, prominent ventricular expansions were detected and we found that these patients had strongest hippocampal atrophy occurring at CA1 and strongest amygdala atrophy at the basolateral complex. Mild atrophy in basal ganglia structures was also detected in MCI and AD. Stronger atrophy in the amygdala and hippocampus, and greater expansion in ventricles was observed in MCI converters, relative to those MCI who remained stable. Furthermore, we performed principal component analysis on a linear shape space of each structure. A subsequent linear discriminant analysis on the principal component values of hippocampus, amygdala, and ventricle leads to correct classification of 88% HC subjects and 86% AD subjects.

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MRI-derived entorhinal and hippocampal atrophy in incipient and very mild Alzheimer’s disease ☆ ☆This research was supported by grants P01 AG09466 and P30 AG10161 from the National Institute on Aging, National Institutes of Health.

Cited by 426 publications

References 45 publications

Hippocampal disconnection contributes to memory dysfunction in individuals at risk for Alzheimer’s disease

Hippocampal disconnection contributes to memory dysfunction in individuals at risk for Alzheimer’s disease

Role of Amyloid from a Multiple Sclerosis Perspective: A Literature Review

Shape abnormalities of subcortical and ventricular structures in mild cognitive impairment and Alzheimer's disease: Detecting, quantifying, and predicting

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