Cerebrospinal Fluid Anti-Amyloid-β Autoantibodies and Amyloid PET in Cerebral Amyloid Angiopathy-Related Inflammation

2015 ◽  
Vol 50 (1) ◽  
pp. 1-7 ◽  
Author(s):  
María Carmona-Iragui ◽  
Ana Fernández-Arcos ◽  
Daniel Alcolea ◽  
Fabrizio Piazza ◽  
Estrella Morenas-Rodriguez ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Cerebral Amyloid Angiopathy ◽  
Amyloid Β ◽  
Amyloid Angiopathy ◽  
Amyloid Pet ◽  
Cerebral Amyloid

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.

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.

scholarly journals Cerebrospinal fluid biomarkers and apolipoprotein E genotype in cerebral amyloid angiopathy. A narrative review

2021 ◽  
Vol 2 ◽  
pp. 100010
Author(s):  
Aikaterini Theodorou ◽  
Ioanna Tsantzali ◽  
Elisabeth Kapaki ◽  
Vasilios C. Constantinides ◽  
Konstantinos Voumvourakis ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Apolipoprotein E ◽  
Cerebral Amyloid Angiopathy ◽  
Narrative Review ◽  
Amyloid Angiopathy ◽  
Cerebrospinal Fluid Biomarkers ◽  
Cerebral Amyloid ◽  
Apolipoprotein E Genotype

scholarly journals Cerebral amyloid angiopathy severity is linked to dilation of juxtacortical perivascular spaces

2015 ◽  
Vol 36 (3) ◽  
pp. 576-580 ◽  
Author(s):  
Susanne J van Veluw ◽  
Geert Jan Biessels ◽  
Willem H Bouvy ◽  
Wim GM Spliet ◽  
Jaco JM Zwanenburg ◽  
...  
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Small Vessel Disease ◽  
Amyloid Β ◽  
Amyloid Angiopathy ◽  
Perivascular Spaces ◽  
Resonance Imaging ◽  
Centrum Semiovale ◽  
Tissue Sections ◽  
Cortical Areas ◽  
Cerebral Amyloid

Perivascular spaces are an emerging marker of small vessel disease. Perivascular spaces in the centrum semiovale have been associated with cerebral amyloid angiopathy. However, a direct topographical relationship between dilated perivascular spaces and cerebral amyloid angiopathy severity has not been established. We examined this association using post-mortem magnetic resonance imaging in five cases with evidence of cerebral amyloid angiopathy pathology. Juxtacortical perivascular spaces dilation was evaluated on T2 images and related to cerebral amyloid angiopathy severity in overlying cortical areas on 34 tissue sections stained for Amyloid β. Degree of perivascular spaces dilation was significantly associated with cerebral amyloid angiopathy severity (odds ratio = 3.3, 95% confidence interval 1.3–7.9, p = 0.011). Thus, dilated juxtacortical perivascular spaces are a promising neuroimaging marker of cerebral amyloid angiopathy severity.

Amyloid-PET in cerebral amyloid angiopathy

Neurology ◽  
2017 ◽  
Vol 89 (14) ◽  
pp. 1437-1438 ◽  
Author(s):  
Nicolas Raposo ◽  
Joshua A. Sonnen
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Amyloid Angiopathy ◽  
Amyloid Pet ◽  
Cerebral Amyloid

scholarly journals Evidence of amyloid-β cerebral amyloid angiopathy transmission through neurosurgery

2018 ◽  
Vol 135 (5) ◽  
pp. 671-679 ◽  
Author(s):  
Zane Jaunmuktane ◽  
Annelies Quaegebeur ◽  
Ricardo Taipa ◽  
Miguel Viana-Baptista ◽  
Raquel Barbosa ◽  
...  
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Amyloid Β ◽  
Amyloid Angiopathy ◽  
Cerebral Amyloid

Vessels Sing Their ARIAs: The Role of Vascular Amyloid in the Age of Aducanumab

Stroke ◽  
2021 ◽  
Author(s):  
Lukas Sveikata ◽  
Andreas Charidimou ◽  
Anand Viswanathan
Keyword(s):  
Clinical Trials ◽  
Alzheimer Disease ◽  
Cerebral Amyloid Angiopathy ◽  
Amyloid Β ◽  
High Rate ◽  
Amyloid Angiopathy ◽  
Cerebrovascular Pathology ◽  
Cerebral Amyloid

We review the implications of the recently approved aducanumab amyloid-β immunotherapy for treating Alzheimer disease with comorbid cerebral amyloid angiopathy. In clinical trials, amyloid-β immunotherapy has been associated with a high rate of amyloid-related imaging abnormalities, potentially driven by coexisting cerebral amyloid angiopathy. Therefore, immunotherapy’s efficacy in patients may be modified by coexisting cerebrovascular pathology. We discuss the contributions of cerebral amyloid angiopathy on the development of amyloid-related imaging abnormalities and propose strategies to identify cerebral amyloid angiopathy in patients considered for immunotherapy.

MEMANTINE ATTENUATES VASCULAR AMYLOID β DEPOSITS AND SPONTANEOUS HEMORRHAGES IN MOUSE MODELS OF CEREBRAL AMYLOID ANGIOPATHY

2017 ◽  
Vol 13 (7) ◽  
pp. P917-P918 ◽  
Author(s):  
Yasuteru Inoue ◽  
Mitsuharu Ueda ◽  
Teruaki Masuda ◽  
Yohei Misumi ◽  
Taro Yamashita ◽  
...  
Keyword(s):  
Mouse Models ◽  
Cerebral Amyloid Angiopathy ◽  
Amyloid Β ◽  
Amyloid Angiopathy ◽  
Cerebral Amyloid
Sign in / Sign up

Export Citation Format

Share Document