Increased Apolipoprotein E mRNA in the Hippocampus in Alzheimer Disease and in Rats after Entorhinal Cortex Lesioning

Zarow, Chris; Victoroff, Jeff

doi:10.1006/exnr.1997.6709

Cited by 52 publications

(24 citation statements)

References 50 publications

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“…On the other hand, there are few reports on the quantitative change of apoE, namely the expression of apoE mRNA in AD. It has been reported that the skin fibroblast apoE mRNA level may decrease in AD patients [1], while that the brain apoE mRNA level may increase or decrease in AD patients [6][7][8]. These previous studies were small sized, and the results were not consistent.…”

Section: Introductioncontrasting

confidence: 46%

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

Yamagata

Urakami

Ikeda

et al. 2001

Dement Geriatr Cogn Disord

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In order to study progressive dementia in Alzheimer’s disease (AD) patients, we analyzed the gene expression of apolipoprotein E (apoE). ApoE mRNA level in the brains of patients with AD was determined by the reverse transcriptase-polymerase chain reaction (RT-PCR) method. ApoE genotype and the promoter polymorphisms (–491A/T, Th1/E47cs) were determined by the PCR restriction fragment length polymorphism method. The apoE mRNA level was significantly higher in the AD group than the control group (p < 0.05). ApoE mRNA in the AD group with apoE Ε4 was also significantly higher than that in the control group with apoE Ε4 (p < 0.05). Our result did not indicate the possibility that the promoter polymorphisms modulate the apoE mRNA level. The higher level of apoE mRNA in AD with apoE Ε4 may play an important role in the development of AD.

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Section: Introductioncontrasting

confidence: 46%

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

Yamagata

Urakami

Ikeda

et al. 2001

Dement Geriatr Cogn Disord

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“…Our observation is consistent with other reports of elevated levels of APOE mRNA in AD brains. For example, Zarow et al report increased APOE mRNA levels in the hippocampus of AD cases compared to controls[24] and Matsui et al report increased APOE mRNA levels in temporal cortex of AD donors compared to controls[25]. Furthermore, Akram et al have recently demonstrated that APOE mRNA and protein levels in the inferior temporal gyrus and the hippocampus are strongly, positively correlated with the progression of cognitive dysfunction[26].…”

Section: Discussionmentioning

confidence: 99%

The cis‐regulatory effect of an Alzheimer's disease‐associated poly‐T locus on expression of TOMM40 and apolipoprotein E genes

Linnertz

Anderson

Gottschalk

et al. 2014

Alzheimer's & Dementia

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Introduction We investigated the TOMM40-APOE genomic region that has been associated with the risk and age of onset of late-onset Alzheimer's disease (LOAD) to determine if a highly polymorphic, intronic polyT within this region (rs10524523, hereafter 523) affects expression of the APOE and TOMM40 genes. Alleles of this locus are classified: short-S, long-L, very long-VL based on the number of T-residues. Methods We evaluated differences in APOE-mRNA and TOMM40-mRNA levels as a function of 523 genotype in two brain regions from APOEε3/3 Caucasian autopsy-confirmed LOAD cases and normal controls. We further investigated the effect of the 523 locus in its native genomic context using a luciferase expression system. Results The expression of both genes was significantly increased with disease. Mean expression of APOE and TOMM40-mRNA levels were higher in VL-homozygotes compared to S-homozygotes in temporal and occipital cortexes from Normal and LOAD subjects. Results of a luciferase reporter system were consistent with the human brain mRNA analysis: the 523-VL polyT resulted in significantly higher expression than the S-polyT. While the effect of polyT length on reporter expression was the same in HepG2 hepatoma and SH-SY5Y neuroblastoma cells, the magnitude of the effect was greater in the neuroblastoma than in the hepatoma cells, which implies tissue-specific modulation of the 523-polyT. Conclusions These results suggest that the 523 locus may contribute to LOAD susceptibility by modulating the expression of TOMM40 and/or APOE transcription.

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“…Although apoE is often increased by inflammatory stimuli, and this can be coordinate with upregulation of the canonical glial reactivity marker GFAP (Poirier et al, 1991;Laping et al, 1994a) (which was downregulated by ibuprofen in these mice (Lim et al, 2000)), in some inflammatory and neurodegenerative conditions apoE mRNA expression is not coordinately regulated with GFAP mRNA (Laping et al, 1994b;Schauwecker et al, 1998;Petegnief et al, 2001), including conditions related to amyloid plaques and AD (Shao et al, 1997;Zarow and Victoroff, 1998). In addition, apoE mRNA is uniquely downregulated by apoE and Ab proteins (Soulie et al, 1999;Yamauchi et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Ibuprofen Suppresses Interleukin-1β Induction of Pro-Amyloidogenic α1-Antichymotrypsin to Ameliorate β-Amyloid (Aβ) Pathology in Alzheimer's Models

Morita

Teter

Yang

et al. 2005

Neuropsychopharmacol

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Epidemiological and basic research suggests that nonsteroidal anti-inflammatory drugs (NSAIDs) should protect against the most common forms of Alzheimer's disease (AD). Ibuprofen reduces amyloid (Ab) pathology in some transgenic models, but the precise mechanisms remain unclear. Although some reports show select NSAIDs inhibit amyloid production in vitro, the possibility that in vivo suppression of amyloid pathology occurs independent of Ab production has not been ruled out. We show that ibuprofen reduced Ab brain levels in rats from exogenously infused Ab in the absence of altered Ab production. To determine whether ibuprofen inhibits proamyloidogenic factors, APPsw (Tg2576) mice were treated with ibuprofen for 6 months, and expression levels of the Ab and inflammation-related molecules a 1 antichymotrypsin (ACT), apoE, BACE1, and peroxisome proliferator-activated receptor g) (PPARg) were measured. Among these, ACT, a factor whose overexpression accelerates amyloid pathology, was reduced by ibuprofen both in vivo and in vitro. IL-1b, which was reduced in our animals by ibuprofen, induced mouse ACT in vitro. While some NSAIDs may inhibit Ab42 production, these observations suggest that ibuprofen reduction of Ab pathology may not be mediated by altered Ab42 production. We present evidence supporting the hypothesis that ibuprofen-dependent amyloid reduction is mediated by inhibition of an alternate pathway (IL-1b and its downstream target ACT).

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Increased Apolipoprotein E mRNA in the Hippocampus in Alzheimer Disease and in Rats after Entorhinal Cortex Lesioning

Cited by 52 publications

References 50 publications

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

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

The cis‐regulatory effect of an Alzheimer's disease‐associated poly‐T locus on expression of TOMM40 and apolipoprotein E genes

Ibuprofen Suppresses Interleukin-1β Induction of Pro-Amyloidogenic α1-Antichymotrypsin to Ameliorate β-Amyloid (Aβ) Pathology in Alzheimer's Models

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