High Expression of Apolipoprotein E mRNA in the Brains with Sporadic Alzheimer’s Disease

Yamagata, Kazuya; Urakami, Katsuya; Ikeda, Kazuyuki; Ji, Yong; Adachi, Yoshiki; Arai, Hiroyuki; Sasaki, Hidetada; Sato, Kei; Nakashima, Kenichiro

doi:10.1159/000051236

Cited by 46 publications

(33 citation statements)

References 24 publications

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“…As such, it presents a plausible explanation for our findings in the frontal cortex. These findings are also supported in the literature by reports that mRNA is increased in the frontal and temporal cortex 18,19 as well as in the hippocampus 20 of neuropathologically confirmed AD cases. It is also supported by findings of increased soluble levels in the cerebellar cortex and increased bound apoE levels in the frontal cortex of AD brains.…”

Section: Resultssupporting

confidence: 85%

Variation at the APOE −491 promoter locus is associated with altered brain levels of apolipoprotein E

et al. 2002

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The apolipoprotein E (APOE, gene; apoE, protein) type 4 isoform is a well-established risk factor for late-onset Alzheimer's disease (AD), and new data suggest that APOE promoter polymorphisms might also modulate AD risk, perhaps by altering transcription of the APOE gene. The current study was undertaken to determine whether the presence of the APOE promoter −491AA genotype (that appears to increase the risk for AD) is associated with an increase in the levels of apoE in brain tissue. Among 40 control and 20 autopsy-confirmed AD brain samples, levels of apoE were increased in the frontal cortex of AD cases (P Ͻ 0.001), consistent with the well-recognized up-regulation of APOE expression in reactive astrocytes. Among controls, the −491A allele appeared to impart a gene dose-dependent effect on the levels of apoE in frontal cortex. The levels of apoE in the brains of AD patients with the −491AA genotype were increased as compared to control subjects with the same genotype (P Ͻ 0.001). These data support the notion that the −491AA APOE promoter genotype is associated with elevated brain apolipoprotein E levels, suggesting that the risk for AD may be modulated by the apoE protein level as well as by the apoE protein isoform.

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Section: Resultssupporting

confidence: 85%

Variation at the APOE −491 promoter locus is associated with altered brain levels of apolipoprotein E

et al. 2002

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“…Whereas an association between -491 AA and AD was further confirmed in subjects who did not carry the APOE Â4 allele [24,25], the association detected in two other studies [26,27] was the result in part of linkage disequilibrium between -491 AA and Â4 alleles. In contrast to these observations, other studies reported no increased risk for AD with the -491 AA genotype in Caucasian [28,29], Japanese [30,31] or Chinese [32] populations. Conversely, it has been suggested that the relationship of the -491 A/T polymorphism with AD is not that of a risk factor but of a possible protective factor, with the TT genotype being associated with a 10-fold decreased risk of having AD [33].…”

Section: Apoecontrasting

confidence: 56%

Candidate Gene Association Studies in Sporadic Alzheimer’s Disease

Combarros

Alvarez-Arcaya²,

Sánchez-Guerra³

et al. 2002

Dement Geriatr Cogn Disord

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The genetics of Alzheimer’s disease (AD) is complex. Three genes (amyloid precursor protein, presenilin 1 and presenilin 2) have been described in the relatively rare, early-onset, autosomal dominant familial form of AD. In the common, non-familial (sporadic) late-onset AD, the major known genetic risk factor is the Ε4 allele of the apolipoprotein E (APOE) gene. However, at least half of the people who develop AD do not carry this allele, and not all people who do carry this allele develop AD even if they live to an old age. Therefore, approximately 30 other candidate genes involving a protein in a critical pathway in the pathogenesis of disease (principally interaction with amyloid-β, oxidative stress and inflammation/apoptosis) have been considered as risk factors for sporadic AD. Then these genes have been sequenced in search of genetic variability or polymorphisms, and each putative polymorphism has been reported to alter the risk of AD either directly or by an interaction with the APOE Ε4 allele. However, positive-association studies with these candidate genes have not been consistently confirmed.

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“…Many types of MI probes have been developed for different MI techniques [13,24,30] . Popular target choices are receptors, enzymes, and cytokines, which are often expressed at a higher level or differently in certain CNS pathologies such as leucine-rich repeat kinase 2 and ␣ -synuclein in Parkinson disease [35,36] or apolipoprotein E in Alzheimer's disease [24,37] . Once such a CNS target is chosen, one needs to select a complementary ligand that binds the target with high affinity and specificity.…”

Section: Cns Targetingmentioning

confidence: 99%

Molecular Imaging for Stem Cell Transplantation in Neuroregenerative Medicine

Sandu¹,

Momen-Heravi²,

Sadr-Eshkevari³

et al. 2011

Neurodegener Dis

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Stem cell transplantation is a promising new therapeutic option in different neurological diseases. However, it was not yet possible to translate its potential from animal models to clinical application. One of the main problems of applying stem cell transplantation in clinical medium is the difficulty of detection, localization, and examination of the stem cells in vivo at both cellular and molecular levels. State-of-the-art molecular imaging techniques provide new and better means for noninvasive, repeated, and quantitative tracking of stem cell implant or transplant. From initial deposition to the survival, migration, and differentiation of the transplant/implanted stem cells, current molecular imaging methods allow monitoring of the infused cells in the same live recipient over time. The present review briefly summarizes and compares these molecular imaging methods for cell labeling and imaging in animal models as well as in clinical application and sheds light on consecutive new therapeutic options if appropriate.

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High Expression of Apolipoprotein E mRNA in the Brains with Sporadic Alzheimer’s Disease

Cited by 46 publications

References 24 publications

Variation at the APOE −491 promoter locus is associated with altered brain levels of apolipoprotein E

Variation at the APOE −491 promoter locus is associated with altered brain levels of apolipoprotein E

Candidate Gene Association Studies in Sporadic Alzheimer’s Disease

Molecular Imaging for Stem Cell Transplantation in Neuroregenerative Medicine

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