Investigation of annexin A5 as a biomarker for Alzheimer's disease using neuronal cell culture and mouse model

Yamaguchi, M.; Kokai, Yasuo; Imai, Shoichi; Utsumi, Kumiko; Matsumoto, Kyoichi; Honda, Hirohito; Mizue, Yuka; Momma, Masako; Maeda, Tetsu; Toyomasu, Shozo; Ito, Yoichi M.; Kobayashi, Seijyu; Hashimoto, Eri; Saito, Toshikazu; Sohma, Hitoshi

doi:10.1002/jnr.22427

Cited by 23 publications

(34 citation statements)

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“…The subjects of this study were 279 control subjects from one of our previous studies [12], 145 patients with probable AD according to the NINCDS/ADRDA criteria [13], and 50 subjects with probable DLB according to the latest consensus diagnostic criteria published in 2005 [11]. To obtain non-demented controls, elderly individuals were recruited in Kitahiroshima, Japan and were evaluated by a questionnaire that included an inquiry into past and present illnesses.…”

Section: Methodsmentioning

confidence: 99%

Apolipoprotein E4 Frequencies in a Japanese Population with Alzheimer's Disease and Dementia with Lewy Bodies

et al. 2011

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BackgroundThe apolipoprotein E (APOE) ε4 allele has been reported to be a risk factor for Alzheimer's disease (AD) and dementia with Lewy bodies (DLB). Previous neuropathological studies have demonstrated similar frequencies of the APOE ε4 allele in AD and DLB. However, the few ante-mortem studies on APOE allele frequencies in DLB have shown lower frequencies than post-mortem studies. One reason for this may be inaccuracy of diagnosis. We examined APOE genotypes in subjects with AD, DLB, and a control group using the latest diagnostic criteria and MRI, SPECT, and MIBG myocardial scintigraphy.MethodsThe subjects of this study consisted of 145 patients with probable AD, 50 subjects with probable DLB, and a control group. AD subjects were divided into two groups based on age of onset: early onset AD (EOAD) and late onset AD (LOAD). All subjects had characteristic features on MRI, SPECT, and/or myocardial scintigraphy.ResultsThe rate of APOE4 carrier status was 18.3% and the frequency of the ε4 allele was 9.7% in controls. The rate of APOE4 carrier status and the frequency of the ε4 allele were 47% and 27% for LOAD, 50% and 31% for EOAD, and 42% and 31% for DLB, respectively.ConclusionThe APOE4 genotypes in this study are consistent with previous neuropathological studies suggesting accurate diagnosis of AD and DLB. APOE4 genotypes were similar in AD and DLB, giving further evidence that the ε4 allele is a risk factor for both disorders.

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Section: Methodsmentioning

confidence: 99%

Apolipoprotein E4 Frequencies in a Japanese Population with Alzheimer's Disease and Dementia with Lewy Bodies

et al. 2011

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“…Plasma annexin A5 was quantified using the Chemiluminescent Enzyme Immunoassay (CLEIA) Technique (SphereLight assay) as described (Yamaguchi et al, 2010). Briefly, annexin A5 present in the specimen was trapped by a monoclonal antibody (mAb) against annexin A5 (clone No.…”

Section: Methodsmentioning

confidence: 99%

“…Possibly, Aβ impairs membrane Ca 2+ pumps and enhances Ca 2+ influx through voltage-dependent channels and ionotropic glutamate receptors. Focusing on this mechanism, we identified the Ca 2+ -related protein as a potential biomarker for AD using primary neurons as a cell culture model (Yamaguchi et al, 2010). It was shown that the level of annexin A5 was augmented in both the brain and blood plasma in an AD-model mouse (Tg2576 transgenic mouse), overexpressing mutant human APP (Yamaguchi et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

“…Focusing on this mechanism, we identified the Ca 2+ -related protein as a potential biomarker for AD using primary neurons as a cell culture model (Yamaguchi et al, 2010). It was shown that the level of annexin A5 was augmented in both the brain and blood plasma in an AD-model mouse (Tg2576 transgenic mouse), overexpressing mutant human APP (Yamaguchi et al, 2010). In addition, the plasma level of annexin A5 was significantly increased in AD patients compared to that in a control group ( p -value of less than 0.0001 in the logistic regression analysis), suggesting that annexin A5 is a favorable marker for AD (Yamaguchi et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

“…It was shown that the level of annexin A5 was augmented in both the brain and blood plasma in an AD-model mouse (Tg2576 transgenic mouse), overexpressing mutant human APP (Yamaguchi et al, 2010). In addition, the plasma level of annexin A5 was significantly increased in AD patients compared to that in a control group ( p -value of less than 0.0001 in the logistic regression analysis), suggesting that annexin A5 is a favorable marker for AD (Yamaguchi et al, 2010). As annexin A5 binds both Ca 2+ and lipids, it might have a role to protect against Ca 2+ -induced damage.…”

Section: Introductionmentioning

confidence: 99%

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Evaluation of annexin A5 as a biomarker for Alzheimer's disease and dementia with lewy bodies

Sohma¹,

Imai²,

Takei³

et al. 2013

Front. Aging Neurosci.

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Background: Alzheimer's disease (AD) differs from other forms of dementia in its relation to amyloid beta peptide (Aβ42). Using a cell culture model we previously identified annexin A5, a Ca2+, and phospholipid binding protein, as an AD biomarker. Plasma level of annexin A5 was significantly higher in AD patients compared to that in a control group. On the other hand, AD has been identified to share a number of clinical and pathological features with Dementia with Lewy bodies (DLB). The present study was done to examine whether or not plasma annexin A5 is a specific marker for AD, when being compared with the levels of DLB patients. As Apolipoprotein E (ApoE) gene subtype ε4 (ApoE-ε4) has been noticed as the probable genetic factor for AD, we also examined and compared ApoE genotype in both AD and DLB.Methods: Blood samples were obtained from 150 patients with AD (aged 77.6 ± 6.5 years), 50 patients of DLB (79.4 ± 5.0) and 279 community-dwelling healthy elderly individuals of comparable age and sex (75.6 ± 8.1). All AD patients met NINCDS-ADRDA criteria and all DLB patients were diagnosed as probable DLB according to the latest consensus diagnostic criteria. Quantification was done using the Chemiluminescent Enzyme Immunoassay (CLEIA) Technique (SphereLight assay) using the monoclonal antibodies against annexin A5. DNA genotyping of ApoE was performed by distinguishing unique combinations of Hha1 fragments of PCR-amplified genomic DNA products.Results: The plasma level of annexin A5 was significantly higher in AD patients than in the healthy individuals (control) (P < 0.0001). The plasma annexin A5 level was also significantly higher in DLB patients than in the control group (P < 0.0001). From the ROC curves with plasma annexin A5 concentrations, the mean areas under the curve were 0.863 and 0.838 for the AD/control and DLB/control, respectively. The rate of ApoE4 carrier status and the frequency of the ε4 allele were significantly higher in AD or DLB than in control and there was no significant difference between AD and DLB.Conclusions: These results suggest that both annexin A5 and ApoE4 are common markers for AD and DLB.

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The Neuroprotective Role of MiR‐124‐3p in a 6‐Hydroxydopamine‐Induced Cell Model of Parkinson's Disease via the Regulation of ANAX5

Dong

Zhang

Tai

et al. 2017

J of Cellular Biochemistry

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Parkinson's disease (PD), the second most common neurodegenerative disorder, is characterized by a progressive loss of dopaminergic neurons in the midbrain. Several pathogenetic factors have been involved in the onset and progression of PD, including inflammation, oxidative stress, unfolded protein accumulation, and apoptosis. Ample evidence indicates that miRNAs could regulate post-transcriptional gene expression and neuronal disease. In this study, we evaluated the effects and mechanism of miR-124-3p on 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in PC12 cells and SH-SY5Y cells. qRT-PCR results showed that the level of miR-124-3p was downregulated in 6-OHDA-treated PC12 and SH-SY5Y cells, and overexpression of miR-124-3p significantly promoted the cell viability of 6-OHDA-treated PC12 and SH-SY5Y cells, whereas miR-124-3p inhibitor reversed these effects. In addition, PC12 or SH-SY5Y cells were treated with miR-124-3p mimics or inhibitors following 6-OHDA administration, which mediated cell apoptosis and downregulation or upregulation of Caspase-3 activity, respectively. A luciferase reporter assay revealed that annexinA5 (ANXA5) is a direct target gene of miR-124-3p, and miR-124-3p overexpression markedly downregulated the level of ANXA5. Strikingly, further analysis showed that miR-124-3p enhanced the viability of 6-OHDA-treated PC12 or SH-SY5Y cells by targeting ANXA5, which was associated with the stimulation of the ERK pathway. This study revealed that miR-124-3p may play a neuroprotective role in PD; this observation may provide new ideas and therapeutic targets for PD.

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Investigation of annexin A5 as a biomarker for Alzheimer's disease using neuronal cell culture and mouse model

Cited by 23 publications

References 41 publications

Apolipoprotein E4 Frequencies in a Japanese Population with Alzheimer's Disease and Dementia with Lewy Bodies

Apolipoprotein E4 Frequencies in a Japanese Population with Alzheimer's Disease and Dementia with Lewy Bodies

Evaluation of annexin A5 as a biomarker for Alzheimer's disease and dementia with lewy bodies

The Neuroprotective Role of MiR‐124‐3p in a 6‐Hydroxydopamine‐Induced Cell Model of Parkinson's Disease via the Regulation of ANAX5

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