Screening for cerebral amyloid angiopathy based on serological biomarkers analysis using a dielectrophoretic force-driven biosensor platform

Lab on a Chip ◽  
2021 ◽  
Author(s):  
Hye Jin Kim ◽  
Dongsung Park ◽  
Gyihyaon Yun ◽  
Hongrae Kim ◽  
Hyug-Gi Kim ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebral Amyloid Angiopathy ◽  
Amyloid Β ◽  
Amyloid Angiopathy ◽  
Dielectrophoretic Force ◽  
Highly Sensitive ◽  
Cerebral Amyloid ◽  
Serological Biomarkers

Screening of cerebral amyloid angiopathy and Alzheimer's disease by analyzing plasma amyloid-β using a highly sensitive dielectrophoretic force-driven biosensor platform.

scholarly journals Cerebrospinal fluid levels of the neurotrophic factor neuroleukin are increased in early Alzheimer’s disease, but not in cerebral amyloid angiopathy

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Anna M. De Kort ◽  
H. Bea Kuiperij ◽  
Daniel Alcolea ◽  
Iris Kersten ◽  
Alexandra A. M. Versleijen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Cerebral Amyloid Angiopathy ◽  
Medical Center ◽  
Senile Plaques ◽  
Amyloid Β ◽  
Amyloid Angiopathy ◽  
Cerebral Amyloid ◽  
Neuro Inflammation

Abstract Background Neuroleukin (NLK) is a protein with neurotrophic properties and is present in a proportion of senile plaques and amyloid laden vessels. It has been suggested that NLK is part of a neuroprotective response to amyloid β-induced cell death. The aim of our study was to investigate the value of cerebrospinal fluid (CSF) NLK levels as a biomarker of vascular amyloid deposition in patients with cerebral amyloid angiopathy (CAA) and in patients with amnestic mild cognitive impairment (aMCI) and Alzheimer’s disease (AD). Methods CSF NLK levels were quantified by ELISA in CAA patients (n = 25) and controls (n = 27) and in two independent samples of aMCI patients, AD patients, and controls: (1) From the Radboud University Medical Center (Nijmegen), we included n = 19 aMCI patients, n = 40 AD patients, and n = 32 controls. (2) From the Hospital of Sant Pau (Barcelona), we included n = 33 aMCI patients, n = 17 AD patients, and n = 50 controls. Results CSF NLK levels were similar in CAA patients and controls (p = 0.95). However, we found an elevated CSF concentration of NLK in aMCI (p < 0.0001) and AD patients (p < 0.0001) compared to controls in both samples sets. In addition, we found a correlation of CSF NLK with CSF YKL-40 (age-adjusted-spearman-rank-coefficient = 0.82, p < 0.0001) in aMCI/AD patients, a well-known glial marker of neuro-inflammation. Conclusions We found that CSF NLK levels are elevated in aMCI and AD patients compared to controls, but are not increased in CAA patients. CSF NLK levels may be related to an increased neuroinflammatory state in early stages of AD, given its association with YKL-40.

scholarly journals Potential Therapeutic Approaches for Cerebral Amyloid Angiopathy and Alzheimer’s Disease

2020 ◽  
Vol 21 (6) ◽  
pp. 1992 ◽  
Author(s):  
Masashi Tanaka ◽  
Satoshi Saito ◽  
Takayuki Inoue ◽  
Noriko Satoh-Asahara ◽  
Masafumi Ihara
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebral Amyloid Angiopathy ◽  
Amyloid Β ◽  
Predictive Biomarkers ◽  
Bioactive Molecules ◽  
Soluble Form ◽  
Amyloid Angiopathy ◽  
Therapeutic Approaches ◽  
Cerebral Amyloid

Cerebral amyloid angiopathy (CAA) is a cerebrovascular disease directly implicated in Alzheimer’s disease (AD) pathogenesis through amyloid-β (Aβ) deposition, which may cause the development and progression of dementia. Despite extensive studies to explore drugs targeting Aβ, clinical benefits have not been reported in large clinical trials in AD patients or presymptomatic individuals at a risk for AD. However, recent studies on CAA and AD have provided novel insights regarding CAA- and AD-related pathogenesis. This work has revealed potential therapeutic targets, including Aβ drainage pathways, Aβ aggregation, oxidative stress, and neuroinflammation. The functional significance and therapeutic potential of bioactive molecules such as cilostazol and taxifolin have also become increasingly evident. Furthermore, recent epidemiological studies have demonstrated that serum levels of a soluble form of triggering receptor expressed on myeloid cells 2 (TREM2) may have clinical significance as a potential novel predictive biomarker for dementia incidence. This review summarizes recent advances in CAA and AD research with a focus on discussing future research directions regarding novel therapeutic approaches and predictive biomarkers for CAA and AD.

Cerebral Amyloid Angiopathy Pathology and Its Association With Amyloid-β PET Signal

Neurology ◽  
2021 ◽  
pp. 10.1212/WNL.0000000000012770
Author(s):  
Stuart McCarter ◽  
Timothy G Lesnick ◽  
Val Lowe ◽  
Michelle M. Mielke ◽  
Eleni Constantopoulos M.H.S. ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebral Amyloid Angiopathy ◽  
Pet Imaging ◽  
Mayo Clinic ◽  
Amyloid Β ◽  
Plaque Burden ◽  
Amyloid Angiopathy ◽  
Amyloid Pet ◽  
Cerebral Amyloid

Objective:To determine the contribution of cerebral amyloid angiopathy (CAA) to Pittsburgh compound B (PiB)-PET tracer retention.Methods:Participants from the Mayo Clinic Study of Aging and Mayo Clinic Alzheimer’s Disease Research Center with antemortem PiB-PET imaging for amyloid beta (Aβ) and later underwent autopsy were included in this study. Pathologic regional leptomeningeal, parenchymal, capillary CAA, and Aβ plaque burden were calculated from one hemisphere. Regional lobar amyloid SUVr on PET was calculated from the same hemisphere sampled at autopsy. Single- and multiple-predictor linear-regression models were used to evaluate the relative contributions of pathologically determined regional CAA and Aβ plaques to antemortem PiB-PET SUVr.Results:Forty-one participants (30 male, 11 female) with a mean age at death of 75.7 (10.6) years were included. Twenty-seven (66%) had high PiB signal with a mean of 2.3 (1.2) years from time of PET scan to death; twenty-four (59%) had a pathologic diagnosis of Alzheimer’s disease. On multivariate analysis, CAA was not associated with PiB-PET SUVr while plaques remained associated with PiB-PET SUVr in all regions (all p <0.05). In patients without frequent amyloid plaques, CAA was not associated with PiB-PET in any region.Conclusion:We did not find evidence that pathologically-confirmed regional CAA burden contributes significantly to proximal antemortem regional PiB-PET signal, suggesting that amyloid PET imaging for measurement of cortical amyloid burden is unconfounded by CAA on a lobar level. Whether CAA burden contributes to PiB-PET signal in patients with severe CAA phenotypes, such as lobar hemorrhage, requires further investigation.

[ 18 F]FDG PET may differentiate cerebral amyloid angiopathy from Alzheimer’s disease

2021 ◽  
Author(s):  
Sébastien Bergeret ◽  
Mathieu Queneau ◽  
Mathieu Rodallec ◽  
Emmanuel Curis ◽  
Julien Dumurgier ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebral Amyloid Angiopathy ◽  
Fdg Pet ◽  
Amyloid Angiopathy ◽  
Cerebral Amyloid

Abstract P418: Stroke Admissions and Outcomes Among Cerebral Amyloid Angiopathy and Alzheimer’s Disease in the National Inpatient Sample

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Nandakumar Nagaraja ◽  
Urvish K Patel
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Hospital Mortality ◽  
Cerebral Amyloid Angiopathy ◽  
Amyloid Angiopathy ◽  
Secondary Diagnosis ◽  
National Inpatient Sample ◽  
Admission Rates ◽  
Secondary Outcomes ◽  
Cerebral Amyloid

Background/Purpose: Although cerebral amyloid angiopathy (CAA) and Alzheimer’s Disease (AD) can manifest as separate diseases it can co-exist due to shared amyloid β pathogenic mechanisms. We assessed admission rates and outcomes of ischemic stroke (IS), intracerebral hemorrhage (ICH), and subarachnoid hemorrhage (SAH) among hospitalized patients with a secondary diagnosis of AD and CAA. Methods: Adult patients discharged with a secondary diagnosis of CAA or AD in National Inpatient Sample (NIS) in the years 2016 and 2017 were identified. Admission rates for IS, ICH, and SAH were primary outcomes. In-hospital mortality and discharge to home were secondary outcomes. Multivariate logistic regression analysis was performed to evaluate secondary outcomes with model adjusted for demographics, medical history, hospital characteristics, and Elixhauser comorbidity index. Results: Among 60,609,519 admissions in NIS, 893,834 (1.5%) patients had a secondary diagnosis of AD [mean age 82.1 years and 62% women] and 14,850 (0.02%) patients had CAA [mean age 76.2 years and 51% women]. Combined AD+CAA was present in 1,335 (0.002%) patients. Compared to AD and controls (non AD or CAA), patients with CAA had higher admission rates for IS (11.5% CAA vs 2.8% AD vs 1.7% control, p<0.0001), for ICH (29.5% CAA vs 0.4% AD vs 0.2% control, p<0.0001) and for SAH (3% CAA vs 0.1% AD vs 0.1% control, p<0.0001). Among patients admitted for IS, discharge to home was less likely in AD compared to controls (10.4% AD vs 36.3% control, OR=0.40; 95%CI=0.36-0.44). Among patients admitted for ICH, discharge to home was less likely in AD compared to controls (6.3% AD vs 18.5% control, OR=0.57; 95%CI=0.41-0.78) but higher in CAA (17.8% CAA vs 18.5% control, OR=1.35; 95%CI=1.11-1.63). In-hospital mortality was less likely in patients with CAA than controls among patients admitted for ICH (9.6% CAA vs 23% control, OR=0.33; 95%CI=0.26-0.41) and SAH (6.7% CAA vs 19.1% control, OR=0.27; 95%CI=0.11-0.62). Conclusion: Admissions for IS, ICH, and SAH were higher among CAA compared to AD in NIS. CAA patients had lower in-hospital mortality for ICH and SAH admissions and higher rates of home discharge for ICH admissions. AD patients were less likely to be discharged home for IS and ICH admissions.

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