amyloid/beroerte

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Intravenous immunoglobulin protects neurons against amyloid beta-peptide toxicity and ischemic stroke by attenuating multiple cell death pathways.

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Intravenous immunoglobulin (IVIg) preparations obtained by fractionating blood plasma, are increasingly being used increasingly as an effective therapeutic agent in treatment of several inflammatory diseases. Its use as a potential therapeutic agent for treatment of stroke and Alzheimer's disease

Cerebral amyloid angiopathy related hemorrhage after stroke thrombolysis: case report and literature review.

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Cerebral amyloid angiopathy (CAA) predisposes to symptomatic intracerebral hemorrhage (sICH) after combined thrombolytic and anticoagulant treatment of acute myocardial infarction. However, the role of CAA in stroke thrombolysis has not been established. Here, we describe a confirmed case of

Stroke in Icelandic patients with hereditary amyloid angiopathy is related to a mutation in the cystatin C gene, an inhibitor of cysteine proteases.

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Cystatin C is an inhibitor of lysosomal cysteine proteases and consists of 120 amino acids. A variant of cystatin C lacking the first NH2-terminal residues and having one amino acid substitution at position 68 forms amyloid deposits mainly in the walls of brain arteries, causing fatal strokes in

Ischaemic stroke as the initial manifestation of systemic amyloidosis.

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A previously healthy 54-year-old woman was admitted to the stroke unit with an acute ischaemic stroke attributed to atrial fibrillation newly diagnosed at the emergency room. Nevertheless, preliminary investigation on stroke aetiology revealed incidental hypoalbuminaemia in the context of nephrotic

Interplay between age, cerebral small vessel disease, parenchymal amyloid-β, and tau pathology: longitudinal studies in hypertensive stroke-prone rats.

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BACKGROUND Accumulation of amyloid-β (Aβ) and hyperphosphorylated tau (ptau) accompany cerebral small vessel disease (CSVD) in the aging brain and in Alzheimer's disease. CSVD is characterized by a heterogeneous spectrum of histopathological features possibly initiated by an endothelial dysfunction

Impact of N-Acetylcysteine on cerebral amyloid-β plaques and kidney damage in spontaneously hypertensive stroke-prone rats.

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BACKGROUND Cerebral small vessel disease (CSVD) in spontaneously hypertensive stroke prone rats (SHRSP) is accompanied by parenchymal amyloid-β (Aβ) deposition in the brain and by hypertensive nephropathy with tubulointerstitial damage. N-acetylcysteine (NAC) promotes blood-brain barrier (BBB)

Familial cerebral amyloid angiopathy related to stroke and dementia.

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The term cerebral amyloid angiopathy (CAA) refers to the specific deposition of amyloid fibrils in the walls of leptomeningeal and cortical arteries, arterioles and, although less frequently in capillaries and veins. It is commonly associated with Alzheimers disease, Down's syndrome and normal

Hemorrhagic stroke, cerebral amyloid angiopathy, Down syndrome and the Boston criteria.

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A stroke, or a cerebrovascular accident (CVA) is a life-threatening condition which often results in permanent or significant disability in the adult population. Several classifications of CVAs exist, one of them being based on the mechanism of injury of brain tissue: ischemic (85-90%) and

Cerebral Amyloid Angiopathy: A Different Kind of Stroke.

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When a patient presents with stroke-type symptoms, the correct diagnosis is imperative to determine appropriate treatment. Cerebral amyloid angiopathy (CAA), a buildup of amyloid proteins on the brain artery walls, is a cause of intracerebral hemorrhage. Improved diagnostic criteria and enhanced

Serum amyloid A, fetuin-A, and pentraxin-3 levels in patients with ischemic stroke: novel prognostic biomarkers?

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OBJECTIVE Inflammation plays an important role in acute ischemic stroke. In this study we aimed to investigate the relationship between acute ischemic stroke and serum amyloid A, fetuin-A, and pentraxin-3 which are inflammation markers. METHODS We enrolled 52 patients with acute ischemic stroke and

Amyloidosis complicating the rehabilitation of a patient with a right cerebrovascular accident.

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Physiatrists are rarely presented with a case of amyloidosis. Its unrelenting course must be appreciated in order to speed the process of rehabilitation and help in setting appropriate and rapidly achievable goals. These rehabilitation challenges are discussed with respect to a patient with

Cardiac amyloidosis presenting with recurrent ischaemic strokes.

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A 72-year-old man presented to our service with sudden onset right-sided weakness, aphasia and gaze palsy with diplopia. CT angiogram demonstrated an acute thrombotic occlusion of the distal basilar artery, a basilar infarct and the patient underwent successful thrombectomy. ECG and telemetry

Stroke risk and atrial mechanical dysfunction in cardiac amyloidosis.

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Amyloidosis is associated with poor prognosis, and patients with cardiac involvement have especially poor outcomes. Cardiac amyloidosis leads to higher rates of atrial arrhythmia and an increased risk of intracardiac thrombus formation. However, atrial mechanical dysfunction due to protein

Hemorrhagic stroke associated with the Iowa amyloid precursor protein mutation.

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The authors searched for mutations in the beta-amyloid precursor protein in a Spanish family with a hereditary syndrome of hemorrhagic stroke, dementia, leukoencephalopathy, and occipital calcifications. DNA from two affected members demonstrated the Iowa amyloid precursor protein mutation

White matter alterations following thromboembolic stroke: a beta-amyloid precursor protein immunocytochemical study in rats.

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Thromboembolic stroke in rats leads to a well-described pattern of histopathological and behavioral abnormalities. However, limited data are available in animal models concerning the response of the white matter to embolic events. The purpose of this study was to document patterns of white matter

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