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cerebral amyloid angiopathy/kalín

Krækjan er vistuð á klemmuspjaldið
GreinarKlínískar rannsóknirEinkaleyfi
5 niðurstöður

Pathological studies on cerebral amyloid angiopathy, senile plaques and amyloid deposition in visceral organs in aged dogs.

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The relationship between cerebral lesions such as amyloid angiopathy or senile plaques and amyloid deposition in the visceral organs were studied in 90 autopsy cases of dogs, 0 to 19-year-old. Cerebral amyloid angiopathy was detected in 28 aged dogs (mean age: 13.7-year-old) and was found mostly in

Sporadic cerebral amyloid angiopathy with giant cell reaction.

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We report a case of intracerebral hemorrhages due to sporadic cerebral amyloid angiopathy in a 43-year-old male with a luxuriant giant cell reaction. The amyloid was resistant to potassium permanganate-sulfuric acid oxidation and reacted with an antiserum to synthetic beta-protein. The distribution

Vascular amyloid alters astrocytic water and potassium channels in mouse models and humans with Alzheimer's disease.

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The neurovascular unit (NVU) comprises cerebral blood vessels and surrounding astrocytes, neurons, perivascular microglia and pericytes. Astrocytes associated with the NVU are responsible for maintaining cerebral blood flow and ionic and osmotic balances in the brain. A significant proportion of

Time-course of glial changes in the hyperhomocysteinemia model of vascular cognitive impairment and dementia (VCID).

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Vascular cognitive impairment and dementia (VCID) is the second leading cause of dementia behind Alzheimer's disease (AD) and is a frequent co-morbidity with AD. Despite its prevalence, little is known about the molecular mechanisms underlying the cognitive dysfunction resulting from cerebrovascular

Genome-wide association meta-analysis of neuropathologic features of Alzheimer's disease and related dementias.

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Alzheimer's disease (AD) and related dementias are a major public health challenge and present a therapeutic imperative for which we need additional insight into molecular pathogenesis. We performed a genome-wide association study and analysis of known genetic risk loci for AD dementia using
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