View clinical trials related to Cerebral Amyloid Angiopathy.
Filter by:Cerebral amyloid angiopathy (CAA), caused by amyloid beta depositions in the walls of small cerebral vessels, is remarkably common in the elderly. Its major clinical consequences include intracerebral hemorrhages (ICH) typically in lobar location, functional dependence (disability) and cognitive impairment. Cortical superficial siderosis (cSS) is a common finding in CAA patients and can even be the only magnetic resonance imaging sign of CAA. cSS is of high prognostic relevance regarding future intracerebral haemorrhage and disability. Previous studies suggest that cSS is caused by recurrent focal subarachnoid hemorrhages (fSAH). However, the exact mechanisms and the temporal dynamics of this highly relevant imaging finding are largely unknown. In addition to hemorrhagic manifestations, such as cSS, CAA patients also show ischemic lesions. Of particular interest are acute ischemic lesions as detected by diffusion imaging, which seem to be highly prevalent. Since haemorrhagic and ischemic lesions require fundamentally different therapeutic strategies, understanding the relevance and interplay of both lesion types is highly important for clinical decision making. The HIFI-CAA cohort study aims to provide novel insights into cSS, acute ischemic lesions and other relevant brain alterations in CAA through high-frequency (monthly) serial magnetic resonance imaging.
This is a nested cohort study in the PRO-SVD cohort. Small vessel disease is a chronic disease and is thought to progress over time. MRI is the gold standard to diagnose small vessel disease, but data on MRI-visible disease progression are scarce. Complications of small vessel disease as well as location pattern, distribution and severity of these MRI small vessel disease markers differ according to the underlying phenotype. The primary aim of this project is to investigate individual small vessel disease burden progression detected by MRI in survivors or intracerebral hemorrhage.
Prognosis of small vessel disease (SVD) depends on the underlying type of SVD and index manifestation. The aim of this prospective, observational cohort study is to determine the risk of different outcome events among patients with SVD according to the type of index presentation.
The purpose of this study is to assess safety, tolerability, plasma pharmacokinetics and biologic activity of a single intravenous dose of AMDX-2011P in participants with cerebral amyloid angiopathy (CAA).
We will perform a randomized clinical trial with minocycline. Minocycline is an antibiotic of the tetracycline family and known to modulate inflammation, gelatinase activity and angiogenesis, which we know are central mechanisms in CAA-pathology. Our aim is to prove in a randomized clinical trial in a translational setting that minocycline treatment (duration 3 months) can decrease markers of neuroinflammation and the gelatinase pathway in the cerebrospinal fluid (CSF) of persons with D-CAA (n=30) and sporadic-CAA (n=30).
The overall aim of this pilot study is to investigate the development of magnetic resonance imaging (MRI) and cerebrospinal fluid (CSF) markers after cerebral amyloid angiopathy (CAA)-related and hypertensive arteriopathy (HA)-related intracerebral hemorrhage (ICH) in relation to cognitive decline. The results from this pilot trial will be used to design a larger cohort study to investigate underlying mechanisms of cognitive decline after ICH. The study population consists of 32 patients; 16 patients with CAA-related ICH and 16 patients with HA-related ICH who are 55 years or older. Data will be collected at four measuring points: at baseline (during hospital admission for the ICH or at the outpatients clinic within one month of presentation with an acute ICH), after three months, after six months and after 12 months. Premorbid cognitive functioning will be assessed with the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE) to select participants without pre-existing cognitive impairment.
Cerebral amyloid angiopathy (CAA) is a common form of cerebral small vessel disease, characterized by symptomatic intracerebral hemorrhage and cognitive impairment. However, no effective prevention and treatment strategies have been established. This study aims to evaluate the safety and efficacy of remote ischemic conditioning on patients with CAA.
Cerebral amyloid angiopathy-related intracerebral (CAAH) hemorrhage is second factor of primary intracerebral hemorrhage. However, no effective prevention and treatment strategies have been established. Remote ischemic conditioning is a neuroprotective strategy. In animal studies，RIC is efficiency in accelerating the absorption of hematoma. Therefore, the investigators plan to carry out this research to evaluate the safety and efficacy of RIC in patients with CAA related ICH.
In this three-year proposal, we will explore the MRI-visible EPVS in CAA and investigate its pathophysiology using animal models. Our specific aims include: (1) Establish the relationship of MRI-visible enlarged perivascular space and CAA, (2) Determine whether vascular amyloid clearance in CAA is associated with lymphatic drainage system, (3) Establish longitudinal data for MRI-visible enlarged perivascular space and cerebral amyloid angiopathy progression.
Cerebral amyloid angiopathy (CAA) is one of the major types of cerebral small vessel disease, and a leading cause of spontaneous intracerebral hemorrhage and cognitive decline in elderly patients. Although increasingly detected, a number of aspects including the pathophysiology, the clinical and neuroradiological phenotype and the disease course are still under investigation. The incomplete knowledge of the disease limits the implementation of evidence based guidelines on patient's clinical management and the development of treatments able to prevent or reduce disease progression. The SENECA (SEarchiNg biomarkErs of Cerebral Angiopathy) project is the first Italian multicentre cohort study aimed at better defining the disease natural history and identifying clinical and neuroradiological markers of disease progression. By a multidisciplinary approach and the collection of a large and well phenotyped series and biorepository of CAA patients, the study is ultimately expected to improve the diagnosis and the knowledge of CAA pathophysiological mechanisms.