Density profiles of Alzheimer disease regional brain pathology for the Huddinge brain bank: pattern recognition emulates and expands upon Braak staging

Corder, Elizabeth H.; Woodbury, Max A.; Volkmann, Inga; Madsen, Declan; Bogdanović, Nenad; Winblad, Bengt

doi:10.1016/s0531-5565(00)00147-9

Cited by 54 publications

(37 citation statements)

References 18 publications

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“…Additionally, atrophy was observed in the left and right inferior-medial zone (IMZ), which approximates the underlying subiculum [11] . This pattern of surface shape deformation is consistent with the spatial distribution of neurofibrillary degeneration within the cellular subfields of the hippocampus in patients with pathologically-confirmed AD [1,12] .…”

Section: Introductionsupporting

confidence: 80%

Hippocampal Surface Analysis in Subjective Memory Impairment, Mild Cognitive Impairment and Alzheimer’s Dementia

Tepest

Wang

Csernansky

et al. 2008

Dement Geriatr Cogn Disord

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Background/Aims: Alzheimer’s disease (AD) is preceded by prodromal states. To determine the neuroanatomical basis for the relationship among such states, we assessed surface conformations of the hippocampus in AD, mild cognitive impairment (MCI) and subjective memory impairment (SMI). Methods: Hippocampal surfaces were reconstructed three-dimensionally via large-deformation high-dimensional MRI brain mapping in 14 SMI, 15 MCI, 12 AD and 13 controls. The surfaces were divided a priori into lateral, superior and inferior-medial zones, which approximated the CA1, combined CA2, CA3, CA4 subfields and the subiculum, respectively. Results: Group differences reached statistical significance in the lateral zone (F = 3.2, d.f. = 3, p = 0.033) and inferior-medial zone (F = 2.8, d.f. = 3, p = 0.049) subfields. The groups differed in total hippocampal volume only at the trend level (F = 2.5, d.f. = 3, p = 0.071). Surface deformation maps revealed similar patterns in SMI, MCI and AD subjects, but quantitative differences were significant only when comparing MCI and AD with control subjects. Conclusions: Hippocampal surface deformation in the CA1 subfield was most pronounced in AD, less so in MCI and minor in SMI subjects. These results suggest that hippocampus degeneration develops gradually in AD, and may be observable long before dementia is apparent.

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Section: Introductionsupporting

confidence: 80%

Hippocampal Surface Analysis in Subjective Memory Impairment, Mild Cognitive Impairment and Alzheimer’s Dementia

Tepest

Wang

Csernansky

et al. 2008

Dement Geriatr Cogn Disord

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“…Early in the course of AD, NFTs as well as threads of neurofilaments within dendrites that display cytoskeletal anomalies similar to NFTs appear in the hippocampus, especially within the hippocampal CA1 subfield and subiculum, and gradually increase in density with increasing severity of AD as defined by neuropathological criteria (Braak and Braak, 1991;Corder et al, 2000). There is also a correlation between the density of NFTs in the hippocampus and the severity of dementia as defined by the Clinical Dementia Rating (CDR) scale (Thal et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Abnormalities of hippocampal surface structure in very mild dementia of the Alzheimer type

et al. 2006

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To better define the pattern of hippocampal deformity early in the course of Alzheimer's disease, we compared the pattern of hippocampal surface variation in subjects with very mild dementia of the Alzheimer type (DAT) and nondemented subjects. The surface of the hippocampus was divided a priori on a neuroanatomical template into three zones approximating the locations of underlying subfields [Csernansky, J.G., Wang, L., Swank, J., Miller, J.P., Gado, M., McKeel, D., Miller, M.I., Morris, J.C., 2005. Preclinical detection of Alzheimer's disease: hippocampal shape and volume predict dementia onset in the elderly. NeuroImage 25, 783-792]; i.e., a lateral zone (LZ) approximating the CA1 subfield, a superior zone (SZ) approximating the combined CA2, CA3, CA4 subfields and the gyrus dentatus (GD), and an inferior-medial zone (IMZ) approximating the subiculum. Large-deformation high-dimensional brain mapping (HDBM-LD) was used to generate the hippocampal surfaces of all subjects and to register the surface zones across subjects. Average variations within each zone were calculated for the subjects with very mild DAT as compared to the average of the nondemented subjects. After correcting for multiple comparisons, the very mild DAT subjects showed significant inward variation in the left and right LZ, the left and right IMZ, but not in the left and right SZ as compared to nondemented subjects. In logistic regression analyses, inward variation of the left and right LZ or IMZ by 0.1 mm relative to the average of the nondemented subjects increased the odds of the subject being a very mild DAT subject (range-1.18 to 1.57) rather than being a nondemented subject. The odds ratios for the left and right SZ were not significant. These results represent a replication of our previous findings [Csernansky, J.G., Wang, L., Joshi, S., Miller, J.P., Gado, M., Kido, D., McKeel, D., Morris, J.C., Miller, M.I., 2000. Early DAT is distinguished from aging by high-dimensional mapping of the hippocampus. Neurology 55, 1636-1643.] and suggest that inward deformities of the hippocampal surface in proximity to the CA1

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“…These impairments suggest an early vulnerability of the hippocampus and a subsequent disruption of neocortical networks sustaining consolidated memories (Wiltgen et al, 2004). Although the differential loss of neurons in specific brain regions in AD has been mapped carefully (Braak and Braak, 1991;West et al, 1991;Corder et al, 2000), little is known about the neuronal populations that first become dysfunctional, and even less about the underlying molecular mechanisms. Understanding the processes that cause neuronal dysfunction in AD and related models could guide the development of treatments to prevent AD, preserve learning and memory in its early stages, and maximize cognitive functions in the later stages of the illness.…”

Section: Introductionmentioning

confidence: 99%

Vulnerability of Dentate Granule Cells to Disruption of Arc Expression in Human Amyloid Precursor Protein Transgenic Mice

Palop

Chin²,

Bien-Ly³

et al. 2005

J. Neurosci.

138

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Activity-induced expression of Arc is necessary for maintenance of long-term potentiation and for memory consolidation. In transgenic (TG) mice with neuronal production of human amyloid precursor protein (hAPP) and hAPP-derived amyloid-␤ (A␤) peptides, basal Arc expression was reduced primarily in granule cells of the dentate gyrus. After exploration of a novel environment, Arc expression in these neurons was unaltered in hAPP mice but increased markedly in nontransgenic controls. Other TG neuronal populations showed no or only minor deficits in Arc expression, indicating a special vulnerability of dentate granule cells. The phosphorylation states of NR2B and ERK1/2 were reduced in the dentate gyrus of hAPP mice, suggesting attenuated activity in NMDA-dependent signaling pathways that regulate synaptic plasticity as well as Arc expression. Arc reductions in hAPP mice correlated with reductions in the actin-binding protein ␣-actinin-2, which is located in dendritic spines and, like Arc, fulfills important functions in excitatory synaptic activity. Reductions in Arc and ␣-actinin-2 correlated tightly with reductions in Fos and calbindin, shown previously to reflect learning deficits in hAPP mice. None of these alterations correlated with the extent of plaque formation, suggesting a plaque-independent mechanism of hAPP/A␤-induced neuronal deficits. The brain region-specific depletion of factors that participate in activity-dependent modification of synapses may critically contribute to cognitive deficits in hAPP mice and possibly in humans with Alzheimer's disease.

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Density profiles of Alzheimer disease regional brain pathology for the Huddinge brain bank: pattern recognition emulates and expands upon Braak staging

Cited by 54 publications

References 18 publications

Hippocampal Surface Analysis in Subjective Memory Impairment, Mild Cognitive Impairment and Alzheimer’s Dementia

Hippocampal Surface Analysis in Subjective Memory Impairment, Mild Cognitive Impairment and Alzheimer’s Dementia

Abnormalities of hippocampal surface structure in very mild dementia of the Alzheimer type

Vulnerability of Dentate Granule Cells to Disruption of Arc Expression in Human Amyloid Precursor Protein Transgenic Mice

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