longitudinal biomarker
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2021 ◽  
Vol 12 ◽  
Author(s):  
Panagiotis Ferentinos ◽  
Eirini Maratou ◽  
Anastasia Antoniou ◽  
Alessandro Serretti ◽  
Nikolaos Smyrnis ◽  
...  

Interleukin-1 beta (IL1β) is primarily produced by monocytes in the periphery and the brain. Yet, IL1β protein levels have to date been investigated in major depressive disorder (MDD) and antidepressant response using either plasma or serum assays although with contradictory results, while mononuclear cell assays are lacking despite their extensive use in other contexts. In this pilot study, we comparatively assessed IL1β in mononuclear lysates and plasma in depressed MDD patients over treatment and healthy controls (HC). We recruited 31 consecutive adult MDD inpatients and 25 HC matched on age, sex, and BMI. Twenty-six patients completed an 8-week follow-up under treatment. IL1β was measured in both lysates and plasma in patients at baseline (T0) and at study end (T1) as well as in HC. We calculated ΔIL1β(%) for both lysates and plasma as IL1β percent changes from T0 to T1. Seventeen patients (65.4% of completers) were responders at T1 and had lower baseline BMI than non-responders (p = 0.029). Baseline IL1β from either plasma or lysates could not efficiently discriminate between depressed patients and HC, or between responders and non-responders. However, the two response groups displayed contrasting IL1β trajectories in lysates but not in plasma assays (response group by time interactions, p = 0.005 and 0.96, respectively). ΔIL1β(%) in lysates predicted response (p = 0.025, AUC = 0.81; accuracy = 84.6%) outperforming ΔIL1β(%) in plasma (p = 0.77, AUC=0.52) and was robust to adjusting for BMI. In conclusion, ΔIL1β(%) in mononuclear lysates may be a longitudinal biomarker of antidepressant response, potentially helpful in avoiding untimely switching of antidepressants, thereby warranting further investigation.


Author(s):  
Alessandro Salvalaggio ◽  
Daniele Coraci ◽  
Laura Obici ◽  
Mario Cacciavillani ◽  
Marco Luigetti ◽  
...  

AbstractAxonal polyneuropathy is the main feature of hereditary transthyretin amyloidosis (ATTRv). Nerve morphological abnormalities have been reported, but longitudinal changes have never been assessed. We performed a prospective widespread nerve ultrasound evaluation and nerve cross-sectional area (CSA) was compared with baseline data in both ATTRv patients and pre-symptomatic carriers. Thirty-eight subjects were evaluated (mean follow-up 17.1 months), among them 21 had polyneuropathy while 17 were pre-symptomatic carriers. CSA significantly increased at brachial plexus in both groups (p = 0.008 and p = 0.012) pointing to progressive brachial plexus enlargement as a longitudinal biomarker of both disease progression and disease occurrence in pre-symptomatic carriers.


2021 ◽  
Vol 22 (1) ◽  
Author(s):  
H. Jessen ◽  
N. Hoyer ◽  
T. S. Prior ◽  
P. Frederiksen ◽  
M. A. Karsdal ◽  
...  

Abstract Background Idiopathic pulmonary fibrosis (IPF) is characterized by the accumulation of fibrillar collagens in the alveolar space resulting in reduced pulmonary function and a high mortality rate. Biomarkers measuring the turnover of type I and III collagen could provide valuable information for prognosis and treatment decisions in IPF. Methods Serological biomarkers reflecting the formation of type III collagen (PRO-C3) and degradation of type I (C1M) and III collagen (C3M) were evaluated in a real-world cohort of 178 newly diagnosed IPF patients. Blood samples and clinical data were collected at baseline, six, and 12 months. Baseline and longitudinal biomarker levels were related to disease progression of IPF (defined as ≥ 5% decline in forced vital capacity (FVC) and/or ≥ 10% decline in diffusing capacity for carbon monoxide (DLco) and/or all-cause mortality at 12 months). Furthermore, we analysed differences in percentage change of biomarker levels from baseline between patients receiving antifibrotic treatment or not. Results Increased baseline levels of type I and III collagen turnover biomarkers were associated with a greater risk of disease progression within 12 months compared to patients with a low baseline type I and III collagen turnover. Patients with progressive disease had higher serum levels of C1M (P = 0.038) and PRO-C3 (P = 0.0022) compared to those with stable disease over one year. There were no differences in biomarker levels between patients receiving pirfenidone, nintedanib, or no antifibrotics. Conclusion Baseline levels of type I and III collagen turnover were associated with disease progression within 12 months in a real-world cohort of IPF patients. Longitudinal biomarker levels of type I and III collagen turnover were related to progressive disease. Moreover, antifibrotic therapy did not affect type I and III collagen turnover biomarkers in these patients. PRO-C3 and C1M may be potential biomarkers for a progressive disease behavior in IPF.


2021 ◽  
Author(s):  
Henrik Jessen ◽  
Nils Hoyer ◽  
Thomas Prior ◽  
Peder Frederiksen ◽  
Morten Karsdal ◽  
...  

Abstract Background: Idiopathic pulmonary fibrosis (IPF) is characterized by the accumulation of fibrillar collagens in the alveolar space resulting in reduced pulmonary function and a high mortality rate. Biomarkers measuring the turnover of type I and III collagen could provide valuable information for prognosis and treatment decisions in IPF. Methods: Serological biomarkers reflecting the formation of type III collagen (PRO-C3) and degradation of type I (C1M) and III collagen (C3M) were evaluated in a real-world cohort of 178 newly diagnosed IPF patients. Blood samples and clinical data were collected at baseline, six, and 12 months. Baseline and longitudinal biomarker levels were related to disease progression of IPF (defined as >5% decline in forced vital capacity (FVC) and/or >10% decline in diffusing capacity for carbon monoxide (DLco) and/or all-cause mortality at 12 months). Furthermore, we analysed differences in percentage change of biomarker levels from baseline between patients receiving antifibrotic treatment or not.Results: Increased baseline levels of type I and III collagen turnover biomarkers were associated with a greater risk of disease progression within 12 months compared to patients with a low baseline type I and III collagen turnover. Patients with progressive disease had higher serum levels of C1M (P=0.038) and PRO-C3 (P=0.0022) compared to those with stable disease over one year. There were no differences in biomarker levels between patients receiving pirfenidone, nintedanib, or no antifibrotics. Conclusion: Baseline levels of type I and III collagen turnover were associated with disease progression within 12 months in a real-world cohort of IPF patients. Longitudinal biomarker levels of type I and III collagen turnover were related to progressive disease. Moreover, antifibrotic therapy did not affect type I and III collagen turnover biomarkers in these patients. PRO-C3 and C1M may be potential biomarkers for a progressive disease behavior in IPF.


2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Behnaz Alafchi ◽  
Hossein Mahjub ◽  
Leili Tapak ◽  
Ghodratollah Roshanaei ◽  
Mohammad Ali Amirzargar

In longitudinal studies, clinicians usually collect longitudinal biomarkers’ measurements over time until an event such as recovery, disease relapse, or death occurs. Joint modeling approaches are increasingly used to study the association between one longitudinal and one survival outcome. However, in practice, a patient may experience multiple disease progression events successively. So instead of modeling of a single event, progression of the disease as a multistate process should be modeled. On the other hand, in such studies, multivariate longitudinal outcomes may be collected and their association with the survival process is of interest. In the present study, we applied a joint model of various longitudinal biomarkers and transitions between different health statuses in patients who underwent renal transplantation. The full joint likelihood approaches are faced with the complexities in computation of the likelihood. So, here, we have proposed two-stage modeling of multivariate longitudinal outcomes and multistate conditions to avoid these complexities. The proposed model showed reliable results compared to the joint model in case of joint modeling of univariate longitudinal biomarker and the multistate process.


2021 ◽  
Author(s):  
Wenyi Lin ◽  
Michael C. Donohue ◽  
Philip Insel ◽  
Armin Schwartzman ◽  
Wesley K. Thompson

AbstractAlzheimer’s disease (AD) studies often collect longitudinal biomarker measures of multiple cohorts at different stages of disease and follow these biomarkers with a relatively short period of time. The heterogeneity of the longitudinal patterns of biomarkers can be ubiquitous across both individual trajectories and cognitive domains. We propose a flexible Bayesian multivariate growth mixture model to identify distinct longitudinal patterns of data from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) study. A Gibbs sampling is implemented for achieving the Bayesian inference. We perform a simulation study to demonstrate the adequate performance of our proposed approach and apply the model to identify three latent cognitive decline patterns among patients from the ADNI study.


2020 ◽  
Vol 32 (S1) ◽  
pp. 74-74
Author(s):  
Kai Sin Chin ◽  
Nawaf Yassi ◽  
Zina Hijazi ◽  
Victor Villemagne ◽  
Christopher Rowe ◽  
...  

Background:Cerebral multi-morbidity is common in older people with dementia, including people with dementia with Lewy bodies (DLB). We describe the first Australian-based, longitudinal observational biomarker study of DLB.Aims:To investigate the frequency and influence of Alzheimer’s disease (AD) pathology (amyloid-β and tau) and cerebrovascular disease on clinical symptoms and disease outcome in DLB.Methods:The study will recruit 100 people with mild to moderate probable DLB, who will undergo comprehensive clinical and cognitive assessments. Scales targeting DLB-specific clinical features (such as cognitive fluctuations and rapid eye movement sleep behaviour disorder) are administered. Biomarker protocols incorporate blood sampling (including ApoE genotyping and systemic inflammatory markers), molecular imaging (amyloid-β [18F-NAV 4694], tau [18F-MK6240], VMAT2 [18F-AV133] PET scans), 3-tesla magnetic resonance imaging and optional lumbar puncture. Clinical assessments are completed 6 - monthly and imaging 18-monthly. Participants are also invited to register for post-mortem brain tissue donation.Results:Thirty participants with probable DLB have been enrolled to date (mean age 75.4 years, range 64-82; 87% male). All participants have mild to moderate cognitive impairment (mean MMSE 25, range 17-30). Approximately 64% of the participants were amyloid-β positive. Study procedure tolerability has been excellent with no adverse events reported.Conclusions:There is significant overlap of AD-related proteinopathies in people with DLB. Understanding the impact of multi-morbidity is essential in the development of effective treatment strategies. This study supports the feasibility of intensive, longitudinal biomarker studies in DLB in the Australian setting.


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