P2-232: RELATIONSHIP BETWEEN CEREBRAL AMYLOID ANGIOPATHY AND CSF BIOMARKERS IN DEMENTIA WITH LEWY BODIES

2006 ◽  
Vol 14 (7S_Part_14) ◽  
pp. P759-P759
Author(s):  
Kazutomi Kanemaru ◽  
Akiko Kanemaru ◽  
Shigeo Mutayama ◽  
Aya M. Tokumaru
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Dementia With Lewy Bodies ◽  
Lewy Bodies ◽  
Csf Biomarkers ◽  
Amyloid Angiopathy ◽  
Cerebral Amyloid

Neuropathology

2020 ◽  
pp. 77-98
Author(s):  
Johannes Attems ◽  
Kurt A. Jellinger
Keyword(s):  
Frontotemporal Lobar Degeneration ◽  
Dementia With Lewy Bodies ◽  
Prion Diseases ◽  
Hippocampal Sclerosis ◽  
Neurofibrillary Tangle ◽  
Lewy Bodies ◽  
Corticobasal Degeneration ◽  
Amyloid Angiopathy ◽  
Argyrophilic Grain ◽  
Cerebral Amyloid

This chapter describes the main neuropathological features of the most common age-associated neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, and dementia with Lewy bodies, as well as other less frequent ones such as multiple system atrophy, Pick’s disease, corticobasal degeneration, progressive supranuclear palsy, argyrophilic grain disease, neurofibrillary tangle-dominant dementia, frontotemporal lobar degeneration with TDP-43 pathology, and Huntington’s disease. Likewise, cerebral amyloid angiopathy, hippocampal sclerosis, vascular dementia, and prion diseases are described. A main aim of this chapter is to assist the reader in interpreting neuropathological reports; hence criteria for the neuropathological classifications of the major diseases are provided. One section covers general considerations on neurodegeneration, and basic pathophysiological mechanisms of tau, amyloid-β‎, α‎-synuclein, TDP-43, and prions are briefly described in the sections on the respective diseases. Finally, one section is dedicated to cerebral multimorbidity, and a view on currently emerging neuropathological methods is given.

scholarly journals Core cerebrospinal fluid biomarker profile in cerebral amyloid angiopathy

Neurology ◽  
2018 ◽  
Vol 90 (9) ◽  
pp. e754-e762 ◽  
Author(s):  
Andreas Charidimou ◽  
Jan O. Friedrich ◽  
Steven M. Greenberg ◽  
Anand Viswanathan
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Meta Analysis ◽  
Csf Biomarkers ◽  
Amyloid Angiopathy ◽  
Healthy Controls ◽  
Comparison Groups ◽  
Amyloid Aβ ◽  
Cerebral Amyloid ◽  
T Tau ◽  
Fluid Biomarker

ObjectiveTo perform a meta-analysis of 4 core CSF biomarkers (β-amyloid [Aβ]42, Aβ40, total tau [t-tau], and phosphorylated tau [p-tau]) to assess which of these are most altered in sporadic cerebral amyloid angiopathy (CAA).MethodsWe systematically searched PubMed for eligible studies reporting data on CSF biomarkers reflecting amyloid precursor protein metabolism (Aβ42, Aβ40), neurodegeneration (t-tau), and tangle pathology (p-tau) in symptomatic sporadic CAA cohorts vs controls and patients with Alzheimer disease (AD). Biomarker performance was assessed in random-effects meta-analysis based on ratio of mean (RoM) biomarker concentrations: (1) in patients with CAA vs healthy controls and (2) in patients with CAA vs patients with AD. RoM >1 indicates higher biomarker concentration in patients with CAA vs comparison population and RoM <1 indicates higher concentration in comparison groups.ResultsThree studies met inclusion criteria. These comprised 5 CAA patient cohorts (n = 59 patients) vs healthy controls (n = 94 cases) and AD cohorts (n = 158). Three core biomarkers differentiated CAA from controls: CSF Aβ42 (RoM 0.49, 95% confidence interval [CI] 0.38–0.64, p < 0.003), Aβ40 (RoM 0.70, 95% CI 0.63–0.78, p < 0.0001), and t-tau (RoM 1.54, 95% CI 1.15–2.07, p = 0.004); p-tau was marginal (RoM 1.24, 95% CI 0.99–1.54, p = 0.062). Differentiation between CAA and AD was strong for CSF Aβ40 (RoM 0.76, 95% CI 0.69–0.83, p < 0.0001), but not Aβ42 (RoM 1.00; 95% CI 0.81–1.23, p = 0.970). For t-tau and p-tau, average CSF ratios in patients with CAA vs patients with AD were 0.63 (95% CI 0.54–0.74, p < 0.0001) and 0.60 (95% CI 0.50–0.71, p < 0.0001), respectively.ConclusionSpecific CSF patterns of Aβ42, Aβ40, t-tau, and p-tau might serve as molecular biomarkers of CAA, but analyses in larger CAA cohorts are needed.

scholarly journals β-Amyloid in CSF

Neurology ◽  
2016 ◽  
Vol 88 (2) ◽  
pp. 169-176 ◽  
Author(s):  
Ellis S. van Etten ◽  
Marcel M. Verbeek ◽  
Jeroen van der Grond ◽  
Ronald Zielman ◽  
Sanneke van Rooden ◽  
...  
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Clinical Symptoms ◽  
White Matter Hyperintensity ◽  
Superficial Siderosis ◽  
Csf Biomarkers ◽  
Amyloid Angiopathy ◽  
Cross Sectional ◽  
Mutation Carriers ◽  
Β Amyloid ◽  
Cerebral Amyloid

Objective:To investigate CSF biomarkers in presymptomatic and symptomatic mutation carriers with hereditary cerebral hemorrhage with amyloidosis–Dutch type (HCHWA-D), a model for sporadic cerebral amyloid angiopathy, and to determine the earliest deposited form of β-amyloid (Aβ).Methods:HCHWA-D mutation carriers and controls were enrolled in the cross-sectional EDAN (Early Diagnosis of Amyloid Angiopathy Network) study. The HCHWA-D group was divided into symptomatic carriers with a previous intracerebral hemorrhage and presymptomatic carriers. CSF concentrations of Aβ40, Aβ42, total tau, and phosphorylated tau181 proteins were compared to those of controls of a similar age. Correlations between CSF biomarkers, MRI markers, and age were investigated with multivariate linear regression analyses.Results:We included 10 symptomatic patients with HCHWA-D (mean age 55 ± 6 years), 5 presymptomatic HCHWA-D carriers (mean age 36 ± 13 years), 31 controls <50 years old (mean age 31 ± 7 years), and 50 controls ≥50 years old (mean age 61 ± 8 years). After correction for age, CSF Aβ40 and Aβ42 were significantly decreased in symptomatic carriers vs controls (median Aβ40 1,386 vs 3,867 ng/L, p < 0.001; median Aβ42 289 vs 839 ng/L, p < 0.001) and in presymptomatic carriers vs controls (median Aβ40 3,501 vs 4,684 ng/L, p = 0.011; median Aβ42 581 vs 1,058 ng/L, p < 0.001). Among mutation carriers, decreasing CSF Aβ40 was associated with higher lobar microbleed count (p = 0.010), increasing white matter hyperintensity volume (p = 0.008), and presence of cortical superficial siderosis (p = 0.02).Conclusions:Decreased levels of CSF Aβ40 and Aβ42 occur before HCHWA-D mutation carriers develop clinical symptoms, implicating vascular deposition of both Aβ species as early steps in cerebral amyloid angiopathy pathogenesis. CSF Aβ40 and Aβ42 may serve as preclinical biomarkers of cerebral amyloid angiopathy pathology.

[P2-213]: RELATIONSHIP BETWEEN CEREBRAL AMYLOID ANGIOPATHY AND CSF BIOMARKERS IN ALZHEIMER's DISEASE

2017 ◽  
Vol 13 (7S_Part_14) ◽  
pp. P692-P692
Author(s):  
Kazutomi Kanemaru ◽  
Akiko Kanemaru ◽  
Shigeo Murayama ◽  
Aya M. Tokumaru
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebral Amyloid Angiopathy ◽  
Csf Biomarkers ◽  
Amyloid Angiopathy ◽  
Cerebral Amyloid

scholarly journals Cerebral Amyloid Angiopathy-Related Atraumatic Convexal Subarachnoid Hemorrhage: An ARIA before the Tsunami

2015 ◽  
Vol 35 (5) ◽  
pp. 710-717 ◽  
Author(s):  
Eva Martínez-Lizana ◽  
María Carmona-Iragui ◽  
Daniel Alcolea ◽  
Manuel Gómez-Choco ◽  
Eduard Vilaplana ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Amyloid Angiopathy ◽  
Functional Disability ◽  
Superficial Siderosis ◽  
Csf Biomarkers ◽  
Amyloid Angiopathy ◽  
Cerebral Amyloid ◽  
Convexal Subarachnoid Hemorrhage

Atraumatic convexal subarachnoid hemorrhage (cSAH) in elderly patients is a rare entity that has been associated with cerebral amyloid angiopathy (CAA) and intracerebral hematomas (ICH). To characterize this entity and to study these associations, 22 patients over 60 with cSAH were included in a multicenter ambispective cohort study. Clinical data, magnetic resonance imaging (MRI) studies, APOE genotyping, and cerebrospinal fluid (CSF) biomarkers were evaluated. Results were compared with data from healthy controls (HC), non-cSAH CAA patients (CAAo), and Alzheimer disease patients. Convexal subarachnoid hemorrhage presented with transient sensory or motor symptoms. At follow-up (median 30.7 months), 5 patients had died, 6 survivors showed functional disability (modified Rankins Scale (mRS) > 2), and 12 cognitive impairment. Four patients had prior ICH and six had an ICH during follow-up. CSF-Aβ40 and Aβ42 levels were lower in cSAH and CAAo compared with HC. Convexal subarachnoid hemorrhage presented an APOE-ε2 overrepresentation and CAAo had an APOE-ε4 overrepresentation. On MRI, all patients fulfilled CAA-modified Boston criteria and 9 showed cortical ischemia in the surrounding cortex or the vicinity of superficial siderosis. The neuropathologic study, available in one patient, showed severe CAA and advanced Alzheimer-type pathology. Convexal subarachnoid hemorrhage in the elderly is associated with cognitive impairment and lobar ICH occurrence. Our findings support the existence of an underlying CAA pathology.

scholarly journals The microvascular extracellular matrix in brains with Alzheimer’s disease neuropathologic change (ADNC) and cerebral amyloid angiopathy (CAA)

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Mamatha Damodarasamy ◽  
Robert B. Vernon ◽  
Jasmine L. Pathan ◽  
C. Dirk Keene ◽  
Anthony J. Day ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Extracellular Matrix ◽  
Cerebral Amyloid Angiopathy ◽  
Lewy Bodies ◽  
Protein Product ◽  
Amyloid Angiopathy ◽  
Western Blots ◽  
Cerebral Amyloid ◽  
Brain Microvasculature

Abstract Background The microvasculature (MV) of brains with Alzheimer’s disease neuropathologic change (ADNC) and cerebral amyloid angiopathy (CAA), in the absence of concurrent pathologies (e.g., infarctions, Lewy bodies), is incompletely understood. Objective To analyze microvascular density, diameter and extracellular matrix (ECM) content in association with ADNC and CAA. Methods We examined samples of cerebral cortex and isolated brain microvasculature (MV) from subjects with the National Institute on Aging-Alzheimer's Association (NIA-AA) designations of not-, intermediate-, or high ADNC and from subjects with no CAA and moderate-severe CAA. Cases for all groups were selected with no major (territorial) strokes, ≤ 1 microinfarct in screening sections, and no Lewy body pathology. MV density and diameter were measured from cortical brain sections. Levels of basement membrane (BM) ECM components, the protein product of TNF-stimulated gene-6 (TSG-6), and the ubiquitous glycosaminoglycan hyaluronan (HA) were assayed by western blots or HA ELISA of MV lysates. Results We found no significant changes in MV density or diameter among any of the groups. Levels of BM laminin and collagen IV (col IV) were lower in MV isolated from the high ADNC vs. not-ADNC groups. In contrast, BM laminin was significantly higher in MV from the moderate-severe CAA vs. the no CAA groups. TSG-6 and HA content were higher in the presence of both high ADNC and CAA, whereas levels of BM fibronectin and perlecan were similar among all groups. Conclusions Cortical MV density and diameter are not appreciably altered by ADNC or CAA. TSG-6 and HA are increased in both ADNC and CAA, with laminin and col IV decreased in the BM of high ADNC, but laminin increased in moderate-severe CAA. These results show that changes in the ECM occur in AD and CAA, but independently of one another, and likely reflect on the regional functioning of the brain microvasculature.

EVALUATION OF THE UNITED KINGDOM NATIONAL EXTERNAL QUALITY ASSESSMENT SERVICE 2008 (UK NEQAS 2008) GUIDELINES FOR THE DIAGNOSIS OF SUBARACHNOID HEMORRHAGE USING SPECTROPHOTOMETRIC XANTHOCHROMIA: A RETROSPECTIVE STUDY

2009 ◽  
Vol 32 (6S) ◽  
pp. 5
Author(s):  
A Gangloff ◽  
L Nadeau
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Amyloid Angiopathy ◽  
Viral Encephalitis ◽  
Objective Evaluation ◽  
Final Diagnosis ◽  
Amyloid Angiopathy ◽  
The United Kingdom ◽  
Cerebral Amyloid ◽  
The One ◽  
The Uk

Objective: Evaluation of the UK NEQAS 2008 guidelines for the interpretation of spectrophotometric xanthochromia. Method: A search of the laboratory database for all the xanthochromia test results between May 1st 2008 and May 1st 2009 was performed. Medical charts were reviewed for patients of Hôpital de l’Enfant-Jésus (HEJ) that had at least one detectable pigment (bilirubin, oxyhemoglobin, or methemoglobin). Xanthochromia results obtained with 4 different criteria (Chalmers original, Modified Chalmers, Duiser and UK NEQAS 2008) were compared. Results: We reviewed 41 medical charts (2 patients with duplicate lumbar punctures (LP) for a total of 43 LP). For these 41 patients there were 11 positive xanthochromia results, 5 of which were in concordance with a final diagnosis of subarachnoid hemorrhage (SAH). The diagnosis of the 6 other positive xanthochromia results were as follow: meningeal spread of a lymphoma, cerebral amyloid angiopathy, exertional headache, viral encephalitis with a possibility of petechiaes on the cerebral CT and second LP. Interpretation (negative/positive) of 40/43 LP was identical for the 4 methods. 2 LP were positive with Duiser and UK NEQAS 2008 but negative with Chalmers approaches (final diagnosis: SAH and cerebral amyloid angiopathy). 1 LP was positive only by the Duiser method (viral encephalitis). Conclusions: UK NEQAS 2008 guidelines identified all SAH but are sensitive to traumatic and pathologic meningeal lesions. Except for a case of viral encephalitis with a suspicion of cerebral petechiaes on CT, UK NEQAS 2008 gave xanthochromia results similar to the one in use at HEJ (Duiser). Chalmers original and Modified Chalmers methods missed one of the five SAH.

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