Chronic treatment with five vascular risk factors causes cerebral amyloid angiopathy but no Alzheimer pathology in C57BL/6 mice

2019 ◽  
Vol 7 (Suppl. 1) ◽  
pp. A3.16
Author(s):  
Bettina M. Foidl
Keyword(s):  
Risk Factors ◽  
Cerebral Amyloid Angiopathy ◽  
Chronic Treatment ◽  
Vascular Risk Factors ◽  
Amyloid Angiopathy ◽  
Vascular Risk ◽  
Cerebral Amyloid ◽  
Alzheimer Pathology

scholarly journals Cerebrovascular Risk Factors in Possible or Probable Cerebral Amyloid Angiopathy, Modifier or Bystander?

2021 ◽  
Vol 12 ◽  
Author(s):  
Andrea Wagner ◽  
Jonas Maderer ◽  
Sibylle Wilfling ◽  
Johanna Kaiser ◽  
Mustafa Kilic ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cerebral Amyloid Angiopathy ◽  
Stroke Risk ◽  
Clinical Presentation ◽  
Specific Treatment ◽  
Amyloid Angiopathy ◽  
Stroke Risk Factors ◽  
Cerebrovascular Risk Factors ◽  
Cerebrovascular Risk ◽  
Cerebral Amyloid

Goal: Cerebral amyloid angiopathy (CAA) is a frequent cause of atypical intracerebral hemorrhage (ICH) in the elderly. Stroke risk factors such as arterial hypertension (AHT), atrial fibrillation (AFib), diabetes mellitus (DM), and renal dysfunction (RD) are increasingly apparent in these patients. In this retrospective study, we analyzed the presence of these stroke risk factors in different initial CAA presentations comprising cerebral microbleeds (CMB), acute ischemic stroke (AIS), cortical superficial hemosiderosis (cSS), or lobar ICH (LICH) and evaluated their influence on the initial clinical presentation of patients with CAA.Material and Methods: We identified patients with at least possible CAA defined by the modified Boston criteria admitted to the Department of Neurology or Neurosurgery from 2002 to 2018.Findings: In the overall cohort of 209 patients, we analyzed the correlation between the number of stroke risk factors and the initial clinical presentation of patients with CAA and could show the high multimorbidity of the collective. There are large differences between the subgroups with different initial clinical presentations, e.g., patients with CMB as initial CAA presentation have the highest number of cerebrovascular risk factors and recurrent AIS, whereas AFib is more frequent in the Neurosurgery Department.Conclusion: There is a distinct overlap between the subgroups of CAA manifestations and stroke risk factors that need to be verified in larger patient collectives. Since these comorbidities are likely to influence the clinical course of CAA, they represent possible targets for secondary prevention until specific treatment for CAA becomes available.

scholarly journals Vascular Parkinsonism and Cognitive Impairment without Lobar Hemorrhage related to Cerebral Amyloid Angiopathy

2019 ◽  
pp. 144-148
Author(s):  
FJ Ros Forteza
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Vascular Lesions ◽  
Amyloid Angiopathy ◽  
Vascular Risk ◽  
Vascular Parkinsonism ◽  
Diagnostic Challenge ◽  
Non Invasive ◽  
Lobar Hemorrhage ◽  
Cerebral Amyloid ◽  
Criteria For Diagnosis

Clinical recognition of Cerebral Amyloid Angiopathy is difficult due to clinical and imagiological heterogeneity. The Modified Boston Criteria for diagnosis of ‘probable Cerebral Amyloid Angiopathy’ pathologically validated in 2010 had an increase in sensitivity with only a modest decrease in specificity. Following case illustrates a diagnostic challenge to an elderly patient with vascular risk factors, neurodegenerative symptomatology with multiple cerebral vascular lesions (ischemic and hemorrhagic, without lobar hemorrhage). The use of a non-invasive amyloid marker would be useful in atypical clinical courses of patients with Cerebral Amyloid Angiopathy.

scholarly journals The Role of Basement Membranes in Cerebral Amyloid Angiopathy

2020 ◽  
Vol 11 ◽  
Author(s):  
Matthew D. Howe ◽  
Louise D. McCullough ◽  
Akihiko Urayama
Keyword(s):  
Risk Factors ◽  
Cognitive Decline ◽  
Cerebral Amyloid Angiopathy ◽  
Functional Impairment ◽  
Amyloid Β ◽  
Basement Membranes ◽  
Amyloid Angiopathy ◽  
Transport Pathways ◽  
Cerebral Amyloid ◽  
The Brain

Dementia is a neuropsychiatric syndrome characterized by cognitive decline in multiple domains, often leading to functional impairment in activities of daily living, disability, and death. The most common causes of age-related progressive dementia include Alzheimer’s disease (AD) and vascular cognitive impairment (VCI), however, mixed disease pathologies commonly occur, as epitomized by a type of small vessel pathology called cerebral amyloid angiopathy (CAA). In CAA patients, the small vessels of the brain become hardened and vulnerable to rupture, leading to impaired neurovascular coupling, multiple microhemorrhage, microinfarction, neurological emergencies, and cognitive decline across multiple functional domains. While the pathogenesis of CAA is not well understood, it has long been thought to be initiated in thickened basement membrane (BM) segments, which contain abnormal protein deposits and amyloid-β (Aβ). Recent advances in our understanding of CAA pathogenesis link BM remodeling to functional impairment of perivascular transport pathways that are key to removing Aβ from the brain. Dysregulation of this process may drive CAA pathogenesis and provides an important link between vascular risk factors and disease phenotype. The present review summarizes how the structure and composition of the BM allows for perivascular transport pathways to operate in the healthy brain, and then outlines multiple mechanisms by which specific dementia risk factors may promote dysfunction of perivascular transport pathways and increase Aβ deposition during CAA pathogenesis. A better understanding of how BM remodeling alters perivascular transport could lead to novel diagnostic and therapeutic strategies for CAA patients.

scholarly journals Mixed-location cerebral hemorrhage/microbleeds

Neurology ◽  
2017 ◽  
Vol 90 (2) ◽  
pp. e119-e126 ◽  
Author(s):  
Marco Pasi ◽  
Andreas Charidimou ◽  
Gregoire Boulouis ◽  
Eitan Auriel ◽  
Alison Ayres ◽  
...  
Keyword(s):  
Risk Factors ◽  
Clinical Laboratory ◽  
Small Vessel Disease ◽  
Case Fatality ◽  
Recurrence Risk ◽  
Left Ventricular ◽  
Vascular Risk Factors ◽  
Amyloid Angiopathy ◽  
Perivascular Spaces ◽  
Vascular Risk

ObjectiveTo assess the predominant type of cerebral small vessel disease (SVD) and recurrence risk in patients who present with a combination of lobar and deep intracerebral hemorrhage (ICH)/microbleed locations (mixed ICH).MethodsOf 391 consecutive patients with primary ICH enrolled in a prospective registry, 75 (19%) had mixed ICH. Their demographics, clinical/laboratory features, and SVD neuroimaging markers were compared to those of 191 patients with probable cerebral amyloid angiopathy (CAA-ICH) and 125 with hypertensive strictly deep microbleeds and ICH (HTN-ICH). ICH recurrence and case fatality were also analyzed.ResultsPatients with mixed ICH showed a higher burden of vascular risk factors reflected by a higher rate of left ventricular hypertrophy, higher creatinine values, and more lacunes and severe basal ganglia (BG) enlarged perivascular spaces (EPVS) than patients with CAA-ICH (all p < 0.05). In multivariable models mixed ICH diagnosis was associated with higher creatinine levels (odds ratio [OR] 2.5, 95% confidence interval [CI] 1.2–5.0, p = 0.010), more lacunes (OR 3.4, 95% CI 1.7–6.8), and more severe BG EPVS (OR 5.8, 95% CI 1.7–19.7) than patients with CAA-ICH. Conversely, when patients with mixed ICH were compared to patients with HTN-ICH, they were independently associated with older age (OR 1.03, 95% CI 1.02–1.1), more lacunes (OR 2.4, 95% CI 1.1–5.3), and higher microbleed count (OR 1.6, 95% CI 1.3–2.0). Among 90-day survivors, adjusted case fatality rates were similar for all 3 categories. Annual risk of ICH recurrence was 5.1% for mixed ICH, higher than for HTN-ICH but lower than for CAA-ICH (1.6% and 10.4%, respectively).ConclusionsMixed ICH, commonly seen on MRI obtained during etiologic workup, appears to be driven mostly by vascular risk factors similar to HTN-ICH but demonstrates more severe parenchymal damage and higher ICH recurrence risk.

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