Abstract
C-reactive protein (CRP) participates in the systemic response to inflammation. Previous
studies report inconsistent findings regarding the relationship between plasma CRP
and Alzheimer's disease (AD). We measured plasma CRP in 203 subjects with AD, 58 subjects
with mild cognitive impairment (MCI) and 117 normal aging subjects and administered
annual Mini-Mental State Examinations (MMSE) during a 3-year follow-up period to investigate
CRP's relationship with diagnosis and progression of cognitive decline. Adjusted for
age, sex, and education, subjects with AD had significantly lower levels of plasma
CRP than subjects with MCI and normal aging. However, there was no significant association
between plasma CRP at baseline and subsequent cognitive decline as assessed by longitudinal
changes in MMSE score. Our results support previous reports of reduced levels of plasma
CRP in AD and indicate its potential utility as a biomarker for the diagnosis of AD.
Keywords
To read this article in full you will need to make a payment
Purchase one-time access:
Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online accessOne-time access price info
- For academic or personal research use, select 'Academic and Personal'
- For corporate R&D use, select 'Corporate R&D Professionals'
Subscribe:
Subscribe to Journal of the Neurological SciencesAlready a print subscriber? Claim online access
Already an online subscriber? Sign in
Register: Create an account
Institutional Access: Sign in to ScienceDirect
References
- Inflammation and Alzheimer's disease.in: Neurobiology of Aging. 21(3). Elsevier, 2000: 383-421
- Inflammatory proteins in plasma and the risk of dementia: the Rotterdam study.Arch Neurol. May 2004; 61: 668-672
- C-reactive Protein.J Biol Chem. Nov 19 2004; 279: 48487-48490
- C-reactive protein and IL-6: new marker proteins for the diagnosis of CJD in plasma?.Transfusion. Dec 2001; 41: 1509-1514
- Protective molecules–C-reactive protein (CRP), serum amyloid P (SAP), pentraxin3 (PTX3), mannose-binding lectin (MBL), and apolipoprotein A1 (Apo A1), and their autoantibodies: prevalence and clinical significance in autoimmunity.J Clin Immunol. Nov 2005; 25: 582-591
- Demonstration of CRP immunoreactivity in brains of Alzheimer's disease: immunohistochemical study using formic acid pretreatment of tissue sections.Neurosci Lett. Aug 15 1994; 177: 23-26
- Early inflammation and dementia: a 25-year follow-up of the Honolulu-Asia Aging Study.Ann Neurol. Aug 2002; 52: 168-174
- C-reactive protein: vascular risk marker in elderly patients with mental illness.Dement Geriatr Cogn Disord. Jan 2008; 26: 251-256
- C-reactive protein level is decreased in patients with Alzheimer's disease and related to cognitive function and survival time.Clin Biochem. Oct 2011; 44: 1205-1208
- Decreased C-reactive protein levels in Alzheimer disease.J Geriatr Psychiatry Neurol. Mar 2010; 23: 49-53
- Increased plasma levels of interleukin-1, interleukin-6 and α-1-antichymotrypsin in patients with Alzheimer's disease: peripheral inflammation or signals from the brain?.J Neuroimmunol. Feb 2000; 103: 97-102
- Plasma multianalyte profiling in mild cognitive impairment and Alzheimer disease.Neurology. Aug 28 2012; 79: 897-905
- Clinical diagnosis of Alzheimer´s disease: Report of the NINCDS-ADRDA Work group under the auspices of department of health and human services task force on Alzheimer´s diesease.Neurology. 1984; 34: 939-944
- Random-effects Models for Longitudinal Data.Biometrics. 1982; 38: 963-974
- The apolipoprotein E polymorphism is associated with circulating C-reactive protein (the Ludwigshafen risk and cardiovascular health study).Eur Heart J. Dec 2004; 25: 2109-2119
- Amyloid mediates the association of apolipoprotein E e4 allele to cognitive function in older people.J Neurol Neurosurg Psychiatry. Sep 2005; 76: 1194-1199
Article info
Publication history
Published online: August 26, 2013
Accepted:
May 23,
2013
Received in revised form:
May 19,
2013
Received:
December 28,
2012
Identification
Copyright
© 2013 Elsevier B.V. Published by Elsevier Inc. All rights reserved.