Serum Uric Acid and High-Sensitivity C-Reactive Protein as Predictors of Cognitive Impairment in Patients with Cerebral Infarction

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Abstract

Background: Cognitive impairment induced by cerebral infarction has become a devastating health problem. More efficient predictors are required to evaluate the potential cognitive decline after cerebral infarction in clinic. Serum uric acid (UA) and high-sensitivity C-reactive protein (hs-CRP) are two factors reported to correlate with cognitive impairment. However, the understanding on serum UA and hs-CRP with cognitive dysfunction remains unclear. Methods: Serum UA and hs-CRP were evaluated in patients with cerebral infarction ( n = 197) using single factor analysis and multivariate logistic regression analysis. Clinical and pathological characteristics were analyzed by logistic regression, respectively, and the results demonstrated the correlation between the pathological characteristics and the cognitive impairment post cerebral infarction. Montreal Cognitive Assessment (MoCA) was used to evaluate the patients’ cognitive function, and patients with a MoCA score <26 were recognized as with cognitive impairment. Results: Clinical characteristics related to cognitive impairment, including age, gender, blood pressure, serum UA, and hs-CRP were collected and analyzed. Serum UA and hs-CRP were identified to be potential predictors for post-stroke cognitive dysfunction, with higher serum UA levels correlated with better cognitive function and higher hs-CRP levels correlated with worse cognitive impairment. Conclusion: Serum UA and hs-CRP are two predictors for cognitive impairment post cerebral infarction.

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Most cited references 34

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Oxidative stress and mitochondrial dysfunction in Alzheimer's disease.

So-Hyoung Lee, Wenzhang Wang, Wenzhang Wang … (2014)

Alzheimer's disease (AD) exhibits extensive oxidative stress throughout the body, being detected peripherally as well as associated with the vulnerable regions of the brain affected in disease. Abundant evidence not only demonstrates the full spectrum of oxidative damage to neuronal macromolecules, but also reveals the occurrence of oxidative events early in the course of the disease and prior to the formation of the pathology, which support an important role of oxidative stress in AD. As a disease of abnormal aging, AD demonstrates oxidative damage at levels that significantly surpass that of elderly controls, which suggests the involvement of additional factor(s). Structurally and functionally damaged mitochondria, which are more proficient at producing reactive oxygen species but less so in ATP, are also an early and prominent feature of the disease. Since mitochondria are also vulnerable to oxidative stress, it is likely that a vicious downward spiral involving the interactions between mitochondrial dysfunction and oxidative stress contributes to the initiation and/or amplification of reactive oxygen species that is critical to the pathogenesis of AD. © 2013.

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Dementia and cognitive impairment: epidemiology, diagnosis, and treatment.

Mary Ganguli, Honor J. Hugo (2014)

Symptoms of memory loss are caused by a range of cognitive abilities or a general cognitive decline, and not just memory. Clinicians can diagnose the syndromes of dementia (major neurocognitive disorder) and mild cognitive impairment (mild neurocognitive disorder) based on history, examination, and appropriate objective assessments, using standard criteria such as Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. They can then diagnose the causal subtypes of these syndromes using standard criteria for each of them. Brain imaging and biomarkers are making progress in the differential diagnoses among the different disorders. Treatments are still mostly symptomatic. Copyright © 2014 Elsevier Inc. All rights reserved.

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Is Open Access

Stroke injury, cognitive impairment and vascular dementia☆

Raj Kalaria, Rufus Akinyemi, Masafumi Ihara (2016)

The global burden of ischaemic strokes is almost 4-fold greater than haemorrhagic strokes. Current evidence suggests that 25–30% of ischaemic stroke survivors develop immediate or delayed vascular cognitive impairment (VCI) or vascular dementia (VaD). Dementia after stroke injury may encompass all types of cognitive disorders. States of cognitive dysfunction before the index stroke are described under the umbrella of pre-stroke dementia, which may entail vascular changes as well as insidious neurodegenerative processes. Risk factors for cognitive impairment and dementia after stroke are multifactorial including older age, family history, genetic variants, low educational status, vascular comorbidities, prior transient ischaemic attack or recurrent stroke and depressive illness. Neuroimaging determinants of dementia after stroke comprise silent brain infarcts, white matter changes, lacunar infarcts and medial temporal lobe atrophy. Until recently, the neuropathology of dementia after stroke was poorly defined. Most of post-stroke dementia is consistent with VaD involving multiple substrates. Microinfarction, microvascular changes related to blood–brain barrier damage, focal neuronal atrophy and low burden of co-existing neurodegenerative pathology appear key substrates of dementia after stroke injury. The elucidation of mechanisms of dementia after stroke injury will enable establishment of effective strategy for symptomatic relief and prevention. Controlling vascular disease risk factors is essential to reduce the burden of cognitive dysfunction after stroke. This article is part of a Special Issue entitled: Vascular Contributions to Cognitive Impairment and Dementia edited by M. Paul Murphy, Roderick A. Corriveau and Donna M. Wilcock.

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Author and article information

Journal

Journal ID (publisher-id): DEM

Journal ID (nlm-ta): Dement Geriatr Cogn Disord

Journal ID (doi): 10.1159/issn.1420-8008

Title: Dementia and Geriatric Cognitive Disorders

Publisher: S. Karger AG

ISSN (Print): 1420-8008

ISSN (Electronic): 1421-9824

Publication date Subscription-year: 2020

Publication date (Print): November 2020

Publication date (Electronic): 05 October 2020

Volume: 49

Issue: 3

Pages: 235-242

Affiliations

[_a] _aDivision 2 of Neurology, Cangzhou People’s Hospital, Cangzhou, China

[_b] _bDepartment of Anorectal Surgery, Medical College District of Cangzhou People’s Hospital, Cangzhou, China

[_c] _cDivision 2 of Neurology, Medical College District of Cangzhou People’s Hospital, Cangzhou, China

Author notes

*Linyun Chen, Division 2 of Neurology, Cangzhou People’s Hospital, Qingchi Avenue, Cangzhou 061000 (China), a15511775287@163.com

Article

Publisher ID: 507806 Other ID: Dement Geriatr Cogn Disord 2020;49:235–242

DOI: 10.1159/000507806

PubMed ID: 33017823

SO-VID: e6bbe933-21ae-4325-bd27-cd82a2e65589

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Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

History

Date received : 04 March 2020

Date accepted : 07 April 2020

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Figures: 2, Tables: 3, Pages: 8

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Serum Uric Acid and High-Sensitivity C-Reactive Protein as Predictors of Cognitive Impairment in Patients with Cerebral Infarction

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Abstract

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Karger: Neurology and Neuroscience

Most cited references 34

Oxidative stress and mitochondrial dysfunction in Alzheimer's disease.

Dementia and cognitive impairment: epidemiology, diagnosis, and treatment.

Stroke injury, cognitive impairment and vascular dementia☆

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