C-Reactive Protein Can Be an Early Predictor of Poststroke Apathy in Acute Ischemic Stroke Patients

Chen, Liping; Xiong, Siqing; Liu, Yi; Miao, Lin; Wang, Jirui; Zhong, Renjia; Zhao, Jiuhan; Liu, Wenjing; Zhu, Lu; Shang, Xiuli

doi:10.1016/j.jstrokecerebrovasdis.2018.02.021

Cited by 9 publications

(16 citation statements)

References 28 publications

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“…Changes in dopaminergic neurotransmission may explain associations between apathy and inflammation (Chen et al, 2018;Eurelings et al, 2015). Systemic inflammation can be estimated by circulating plasma C-reactive protein (CRP) levels, which are elevated following an inflammatory response (Pepys and Baltz, 1983).…”

Section: Reward-based Decision-makingmentioning

confidence: 99%

“…Systemic inflammation can be estimated by circulating plasma C-reactive protein (CRP) levels, which are elevated following an inflammatory response (Pepys and Baltz, 1983). Elevated acute phase CRP levels are associated with increasing post-stroke apathy over six months (Chen et al, 2018). Similarly, apathy was correlated with higher CRP levels over several years in community-dwelling individuals (Eurelings et al, 2015).…”

Section: Reward-based Decision-makingmentioning

confidence: 99%

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Network neuroscience of apathy in cerebrovascular disease

Tay

Lisiecka-Ford

Hollocks

et al. 2020

Progress in Neurobiology

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Apathy is a reduction in motivated goal-directed behavior (GDB) that is prevalent in cerebrovascular disease, providing an important opportunity to study the mechanistic underpinnings of motivation in humans. Focal lesions, such as those seen in stroke, have been crucial in developing models of brain regions underlying motivated behavior, while studies of cerebral small vessel disease (SVD) have helped define the connections between brain regions supporting such behavior. However, current lesion-based models cannot fully explain the neurobiology of apathy in stroke and SVD. To address this, we propose a network-based model which conceptualizes apathy as the result of damage to GDB-related networks. A review of the current evidence suggests that cerebrovascular disease-related pathology can lead to network changes outside of initially damaged territories, which may propagate to regions that share structural or functional connections. The presentation and longitudinal trajectory of apathy in stroke and SVD may be the result of these network changes. Distinct subnetworks might support cognitive components of GDB, the disruption of which results in specific symptoms of apathy. This network-based model of apathy may open new approaches for investigating its underlying neurobiology, and presents novel opportunities for its diagnosis and treatment. Recent research on the fundamental neuroanatomical and neurocognitive mechanisms underlying apathy has broadened our understanding of apathy in cerebrovascular disease and across neurological disorders. Despite this, theoretical work has primarily focused on linking neurodegenerative pathology to apathy, such as in Alzheimer's disease or Parkinson's disease (e.g., Lanctôt et al., 2017; Pagonabarraga et al., 2015). This has left the mechanisms underlying apathy in cerebrovascular disease comparably under-explored. Given the high prevalence of comorbid vascular pathology in neurodegenerative

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Section: Reward-based Decision-makingmentioning

confidence: 99%

Section: Reward-based Decision-makingmentioning

confidence: 99%

Network neuroscience of apathy in cerebrovascular disease

Tay

Lisiecka-Ford

Hollocks

et al. 2020

Progress in Neurobiology

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“…In seven RCTs with 657 individuals (322 in the BBR group and 335 in the control group), triglycerides were measured (Chen et al, 2014; Lou et al, 2015; Lu et al, 2018; Wang & Yuan, 2015; Wu, 2016; Yang, 2012; Yang & Chen, 2019). The BBR group had lower levels of triglycerides than the normal control group (WMD = −0.35; 95% CI [−0.55, −0.16], p = 0.0005).…”

Section: Discussionmentioning

confidence: 99%

“…Seven RCTs investigated the effect of the standard treatment plus BBR on LDL‐C levels (Chen et al, 2014; Lou et al, 2015; Lu et al, 2018; Wang & Yuan, 2015; Wu, 2016; Yang, 2012; Yang & Chen, 2019). The meta‐analysis demonstrated a substantial decrease in LDL‐c concentration (WMD = −0.57; 95% CI [−0.76, −0.37], p < 0.00001; Heterogeneity: I 2 = 67%; random‐effect model).…”

Section: Discussionmentioning

confidence: 99%

Effects of adjuvant berberine therapy on acute ischemic stroke: A meta‐analysis

Luo

Sun

et al. 2023

Phytotherapy Research

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We conducted a meta‐analysis to evaluate the clinical efficacy of berberine (BBR) in treating acute ischemic stroke (AIS), explore its anti‐inflammatory effects, and assess its potential applications for AIS patients. We comprehensively searched nine databases from inception until July 1, 2022, to identify clinical trials investigating the use of BBR in treating AIS. We performed statistical analyses using RevMan5.4 software and focused on primary outcomes such as inflammatory markers as well as secondary outcomes including immune system indicators, relevant biomarkers, carotid artery atherosclerosis, and adverse reactions. Our analysis included data from 17 clinical trials involving 1670 patients with AIS. Our results revealed that BBR in combination with conventional treatment significantly reduced levels of high‐sensitivity C‐reactive protein (hs‐CRP), macrophage migration inhibitory factor (MIF), interleukin‐6 (IL‐6), complement C3, hypoxic inducible factor‐1 α (HIF‐1α), cysteine protease‐3 (Caspase‐3), the national institutes of health stroke scale (NIHSS), triglycerides (TG), low‐density lipoprotein cholesterol (LDL‐C), carotid intima‐media thickness (IMT), the number of unstable plaques, and carotid crouse score on ultrasound when compared with conventional treatment alone. Furthermore, combining BBR with conventional treatment may improve the overall effective rate. Therefore, our findings suggest that BBR can be used as an adjuvant therapy for AIS due to its ability to reduce inflammatory cytokine levels, providing a novel therapeutic option for AIS. However, larger randomized controlled trials are necessary to confirm these results.

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“…In a study combining two large national cohorts (National Alzheimer’s Coordinating Center, NACC, n = 22,760 and Alzheimer’s Disease Neuroimaging Initiative, ADNI, n = 1733), lower Aβ 42 was associated with a steep increase in apathy, while higher tau was associated with a marked decrease in apathy over a five-year period [ 69 ]. Among a cohort of stroke patients, post-stroke apathy at six months was significantly associated with elevated C-Reactive Protein (CRP) concentrations [ 70 ]. In a principal component analysis (PCA) study of patients with early Parkinson’s Disease (PD), compared with healthy control subjects, the PC with elevated IL-2 and IL-6 was associated with faster progression of Non-Motor Symptoms Scale total and mood/apathy domain scores [ 71 ].…”

Section: Introductionmentioning

confidence: 99%

The neurobiology of apathy in depression and neurocognitive impairment in older adults: a review of epidemiological, clinical, neuropsychological and biological research

et al. 2022

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Apathy is a common condition that involves diminished initiative, diminished interest and diminished emotional expression or responsiveness. It is highly prevalent in the context of a variety of neuropsychiatric disorders and is related to poor health outcomes. Presence of apathy is associated with cognitive and functional decline in dementia. Despite its negative impact on health, there is no definitive treatment for apathy, a clinical reality that may be due in part to lack of knowledge about assessment, neuropsychological features and neurobiological underpinnings. Here, we review and synthesize evidence from clinical, epidemiological, neuropsychological, peripheral biomarker and neuroimaging research. Apathy is a common feature of depression and cognitive disorders and is associated with impairment in executive function. Neuropsychological and neuroimaging studies point to dysfunction of brain circuitry involving the prefrontal cortex, especially the dorsolateral prefrontal cortex circuit, the dorsomedial prefrontal cortex circuit, and the ventromedial prefrontal cortex circuit. However, inconsistent findings, particularly in neuroimaging may be due to heterogeneity of apathy symptoms (with a need to better elucidate subtypes), neuropsychiatric comorbidities, the severity of cognitive impairment and other factors. These factors need to be accounted for in future studies so that biomarker research can make progress. On the whole, the literature on apathy has identified likely neurocognitive, peripheral biomarker and neuroimaging targets for understanding apathy, but also points to the need to address methodological issues that will better inform future studies. In turn, as we learn more about the underpinning of apathy and its subtypes, subsequent research can focus on new neurally based interventions that will strengthen the clinical management of apathy in the context of its comorbidities.

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C-Reactive Protein Can Be an Early Predictor of Poststroke Apathy in Acute Ischemic Stroke Patients

Cited by 9 publications

References 28 publications

Network neuroscience of apathy in cerebrovascular disease

Network neuroscience of apathy in cerebrovascular disease

Effects of adjuvant berberine therapy on acute ischemic stroke: A meta‐analysis

The neurobiology of apathy in depression and neurocognitive impairment in older adults: a review of epidemiological, clinical, neuropsychological and biological research

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