Serum Amyloid P Component Level in Alzheimer's Disease

Nishiyama, Etsuko; Iwamoto, Norihiko; Kimura, M.; Arai, Heii

doi:10.1159/000106889

Cited by 12 publications

(21 citation statements)

References 10 publications

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“…However, assuming a normal increase in the incidence of AD with age, a high percentage of our centenarians with impaired cognitive performance will in all probability have AD. The results of a recent study by Nishiyama et al [17], reporting a decrease in serum concentration of SAP for 'probable AD' patients, therefore seem to be in disagreement with our findings. One explanation for this discrepancy, although unlikely, would be that only few of the centenarians with a MMSE ^24 have AD, or the inconsistency reflects the difference in the age of the individuals examined.…”

Section: Discussioncontrasting

confidence: 99%

“…The only connection that has been reported so far between SAP concentration and dementia has been SAP's involvement in AD [17,18]. However, assuming a normal increase in the incidence of AD with age, a high percentage of our centenarians with impaired cognitive performance will in all probability have AD.…”

Section: Discussionmentioning

confidence: 98%

“…Amyloidosis occurs frequently in elderly subjects, and the SAP concentration in serum was found to be normal in these and other patients with amyloidosis [14,16]. Recently, however, it was reported [17] that the serum concentration of SAP was significantly lowered in a group of patients with AD, while it was found to be significantly increased in the cerebrospinal fluid in AD patients [18]. In order to investigate whether the SAP concentration was lowered in elderly persons with cognitive impairment, like in the AD patients, the plasma SAP concentration was determined in a group of centenarians and compared to their cognitive performance and to plasma SAP concentrations in a control group of healthy adults.…”

Section: Introductionmentioning

confidence: 99%

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Increased Plasma Concentration of Serum Amyloid P Component in Centenarians with Impaired Cognitive Performance

Nybo¹,

Olsen²,

Jeune³

et al. 1998

Dement Geriatr Cogn Disord

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Serum amyloid P component (SAP) binds to all amyloid fibrils including those in the plaques and tangles of Alzheimer patients. To investigate whether the plasma SAP concentration correlated to cognitive impairment, we measured SAP levels in blood samples from 41 centenarians and compared these to the cognitive performance evaluated by Mini Mental State Examination (MMSE). We observed a significantly (p < 0.001) increased SAP concentration (48.3 ± 16.9 µg/ml; mean ± SD) in the centenarians compared to gender-matched controls (32.8 ± 11.4 µg/ml). Six severely demented centenarians had an even higher SAP concentration (60.2 µg/ml), while the subgroup of cognitive intact centenarians (MMSE score >24) showed a normal SAP concentration (38.4 ± 9.3 µg/ml). No dehydration or hepatic dysfunction was demonstrable in the centenarians. We conclude that the centenarians with impaired cognitive performance had significantly increased plasma concentrations of SAP, while the values for cognitive intact centenarians were within the normal range.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

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Increased Plasma Concentration of Serum Amyloid P Component in Centenarians with Impaired Cognitive Performance

Nybo¹,

Olsen²,

Jeune³

et al. 1998

Dement Geriatr Cogn Disord

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“…154 This effect may be due to an alteration in Ab-binding proteins in AD patients. Previous studies have indicated that there may be alterations in the levels of proteins that attenuate Ab fibrillization, namely a2M 155 and SAP 156 in AD patients, although there are also conflicting data on this issue. It should be noted that polymorphism in the a2M gene may be associated with AD risk in some populations and may be influenced by family history (for example references [157][158][159][160][161][162] ), although these findings are controversial.…”

Section: Ab-binding Proteins In Blood Plasmamentioning

confidence: 99%

Clearance mechanisms of Alzheimer's amyloid-β peptide: implications for therapeutic design and diagnostic tests

et al. 2008

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Currently, the 'amyloid hypothesis' is the most widely accepted explanation for the pathogenesis of Alzheimer's disease (AD). According to this hypothesis, altered metabolism of the amyloid-b (Ab) peptide is central to the pathological cascade involved in the pathogenesis of AD. Although Ab is produced by almost every cell in the body, a physiological function for the peptide has not been determined, and the pathways by which Ab leads to cognitive dysfunction and cell death are unclear. Numerous therapeutic approaches that target the production, toxicity and removal of Ab are being developed worldwide. Although therapeutic treatment for AD may be imminent, the value and effectiveness of such treatment are largely dependent on early diagnosis of the disease. This review summarizes current knowledge of Ab clearance, transport and degradation, and evaluates the use of such information in the development of diagnostic tools. The conflicting results of plasma Ab ELISAs are discussed, as are the more promising results of Ab imaging by positron emission tomography. Current knowledge of Ab-binding proteins and Ab-degrading enzymes is analysed in the context of a potential therapy for AD. Transport across the blood-brain barrier by the receptor for advanced glycation end products and efflux via the multi-ligand lipoprotein receptor LRP-1 is also reviewed. Enhancing clearance and degradation of Ab remains an attractive therapeutic strategy, and improved understanding of Ab clearance may lead to advances in diagnostics and interventions designed to prevent or delay the onset of AD.

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“…The results suggest that the deposition of AP in senile plaques and neurofibrillary tangles is not due to its overproduction. The production of AP by the liver (hepatocytes), Serum Proteome Analysis of Catatonia thought to be the only source, may be suppressed in AD patients [21].…”

Section: Serum Proteome Analysis Of Catatoniamentioning

confidence: 99%

Serum Proteome Analysis of Catatonia

Huang¹,

Lo²,

Lin³

et al. 2017

Neuropsychiatry

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The exact mechanism of catatonia remains a mystery. We tried to investigate the serum biomarkers for patients with catatonia before and after successful treatment using proteomic analysis. During a three-year period, nine patients with schizophrenia who experienced catatonia and nine healthy controls were recruited. 5 ml of venous blood were collected before (acute phase) and after treatment (recovery phase) of catatonia, relieved by intramuscular lorazepam injection. The serum proteomes of acute and recovery phase were compared using two-dimensional polyacrylamide gel electrophoresis (2D-PAGE), combined with matrixassisted laser desorption ionization (MALDI)-time-of-flight (TOF) TOF mass spectrometry (MS). The findings were then validated with enzyme-linked immunosorbent assay (ELISA) by comparing data of patients and healthy controls. Ten differentially expressed protein spots were identified comparing serum proteome profiles of acute phase and recovery phase of catatonia from 2D PAGE. Alpha-2-HS-glycoprotein (AHSG), plasma retinol-binding protein (RBP4) and serum amyloid P component (APCS) may be potential disease-associated biomarkers for catatonia. In the validation phase, those serum proteins were measured in serum of both acute and recovery phase as well as healthy controls with ELISA. Mann-Whitney U-test showed that patients with catatonia in acute phase (p = 0.006) and recovery phase (p = 0.019) both had significantly higher APCS levels than healthy controls. Using ANCOVA with age adjustment, patients with catatonia in acute phase also had significantly higher APCS level than healthy controls (p = 0.048). Our investigation provided a proteomic study in biomarker research of catatonia. APCS might be an important biomaker for the psychopathology in catatonia of schizophrenia. In future, a larger of sample size will be needed to prove these results.

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Serum Amyloid P Component Level in Alzheimer's Disease

Cited by 12 publications

References 10 publications

Increased Plasma Concentration of Serum Amyloid P Component in Centenarians with Impaired Cognitive Performance

Increased Plasma Concentration of Serum Amyloid P Component in Centenarians with Impaired Cognitive Performance

Clearance mechanisms of Alzheimer's amyloid-β peptide: implications for therapeutic design and diagnostic tests

Serum Proteome Analysis of Catatonia

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