amyloid/kanama

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Immunohistochemical characterization of the amyloid deposits and quantitation of pertinent cerebrospinal fluid proteins in hereditary cerebral hemorrhage with amyloidosis.

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Cystatin C, a protein inhibitor of lysosomal cysteine proteinases, was demonstrated by immunohistochemical techniques to be present in the birefringent amyloid deposits of the small arteries in the cerebrum, cerebellum, and leptomeninges of 10 Icelandic individuals with hereditary cerebral

Anti-Amyloid-β Single-Chain Antibody Brain Delivery Via AAV Reduces Amyloid Load But May Increase Cerebral Hemorrhages in an Alzheimer's Disease Mouse Model.

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Accumulation of amyloid-β protein (Aβ) in the brain is thought to be a causal event in Alzheimer's disease (AD). Immunotherapy targeting Aβ holds great promise for reducing Aβ in the brain. Here, we evaluated the efficacy and safety of anti-Aβ single-chain antibody (scFv59) delivery via recombinant

Cortical superficial siderosis and first-ever cerebral hemorrhage in cerebral amyloid angiopathy.

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OBJECTIVE To investigate whether cortical superficial siderosis (cSS) is associated with increased risk of future first-ever symptomatic lobar intracerebral hemorrhage (ICH) in patients with cerebral amyloid angiopathy (CAA) presenting with neurologic symptoms and without ICH. METHODS Consecutive

Amyloid beta protein precursor gene and hereditary cerebral hemorrhage with amyloidosis (Dutch).

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Human hereditary cerebral hemorrhage with amyloidosis of the Dutch type (HCHWA-D), an autosomal dominant form of cerebral amyloid angiopathy (CAA), is characterized by extensive amyloid deposition in the small leptomeningeal arteries and cortical arterioles, which lead to an early death of those

Amyloid beta protein (Abeta) starts to deposit as plasma membrane-bound form in diffuse plaques of brains from hereditary cerebral hemorrhage with amyloidosis-Dutch type, Alzheimer disease and nondemented aged subjects.

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To clarify where and how beta-amyloid begins to deposit in senile plaques, we examined the ultrastructural localization of amyloid beta protein (Abeta) in diffuse plaques of brains with hereditary cerebral hemorrhage with amyloidosis-Dutch type. Alzheimer disease (AD), and from nondemented aged

Colocalization of different types of amyloid in the walls of cerebral blood vessels of patients suffering from cerebral amyloid angiopathy and spontaneous intracranial hemorrhage: a report of 5 cases.

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Four cases of spontaneous intracranial hemorrhage (ICH) are described in which the diagnosis of a cerebral amyloid angiopathy (CAA) was made in the biopsy specimens. In one further case CAA was detected on autopsy after intracranial hemorrhage (ICH). Amyloidotic degeneration of the vessel walls

Intracerebral hemorrhage due to cerebral amyloid angiopathy after head injury: Report of a case and review of the literature.

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Cerebral amyloid angiopathy (CAA) is an important cause of spontaneous intracerebral hemorrhage in the elderly. A few case reports of CAA-related intracerebral hemorrhage after head injury, usually following a fall, have been published. More rarely, it may occur in the setting of a traffic accident,

Cerebrovascular pathology in cerebral amyloid angiopathy presenting as intracerebral haemorrhage.

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Cerebral amyloid angiopathy (CAA) is the second most common cause of non-traumatic intracerebral haemorrhage (ICH) accounting for 12-15% of lobar haemorrhages in the elderly. Definitive diagnosis of CAA requires histological evaluation. We aimed to evaluate the spectrum of cerebrovascular changes in

Bleeding is increased in amyloid precursor protein knockout mouse

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Background: Amyloid precursor protein (APP) is highly expressed in platelets. APP is the precursor to amyloid beta (Aβ) peptides that accumulate in cerebral amyloid angiopathy and plaques in Alzheimer disease. APP and its metabolites

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

Cerebral amyloid-β-related angiitis without cerebral microbleeds in a patient with subarachnoid hemorrhage.

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Amyloid-β-related angiitis (ABRA), a subtype of cerebral amyloid angiopathy (CAA), is vasculitis occurring in relation to amyloid-β (Aβ) deposition in the walls of intracranial blood vessels. ABRA is presumed to be caused by some immune response to the deposited Aβ. An 81-year-old man on oral

Transient focal neurological episodes, cerebral amyloid angiopathy, and intracerebral hemorrhage risk: looking beyond TIAs.

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When most doctors encounter older patients with transient focal neurological symptoms, they usually suspect a diagnosis of transient ischemic attacks or some of their known mimics (including migraine auras or focal seizures). This article emphasizes new observations on transient focal neurological

Role of cerebral amyloid angiopathy in intracerebral hemorrhage in hypertensive patients.

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OBJECTIVE To assess the interaction of cerebral amyloid angiopathy (CAA) and arterial hypertension as cofactors for intracerebral hemorrhage (ICH). METHODS The authors investigated 129 postmortem brains of hypertensive patients with and without ICH. Sixty-four patients had had deep (n = 40) or lobar

Pathological examination of cerebral amyloid angiopathy in patients who underwent removal of lobar hemorrhages.

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Cerebral amyloid angiopathy (CAA) is a degenerative disorder characterized by amyloid-β (Aβ) deposition in the brain microvessels. CAA is also known to contribute not only to cortical microbleeds but also lobar hemorrhages. This retrospective study examined CAA pathologically in patients who

Autopsy of a multiple lobar hemorrhage case with amyloid-β-related angiitis.

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A 92-year-old man died of multiple lobar hemorrhage with amyloid-β protein (Aβ)-related angiitis (ABRA) with an unusual pathological appearance. Although he had shown relatively rapid progressive dementia, starting 1 year before death, there was no detailed clinical investigation, and no

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