cerebral amyloid angiopathy/obesitas

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Prolonged diet induced obesity has minimal effects towards brain pathology in mouse model of cerebral amyloid angiopathy: implications for studying obesity-brain interactions in mice.

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Cerebral amyloid angiopathy (CAA) occurs in nearly every individual with Alzheimer's disease (AD) and Down's syndrome, and is the second largest cause of intracerebral hemorrhage. Mouse models of CAA have demonstrated evidence for increased gliosis contributing to CAA pathology. Nearly two thirds of

Chronic treatment with five vascular risk factors causes cerebral amyloid angiopathy but no Alzheimer pathology in C57BL6 mice.

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Alzheimer's disease (AD) is a progressive neurodegenerative brain disorder and the most common form of dementia coming along with cerebral amyloid angiopathy (CAA) in more than 70% of all cases. However, CAA occurs also in pure form without AD pathology. Vascular life style risk factors such as

Factors associated with lobar vs. non-lobar intracerebral hemorrhage.

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OBJECTIVE The relationship between body mass index (BMI) and stroke subtypes has received more research attention than that between BMI and location of intracerebral hemorrhage (ICH). Lobar hemorrhage (LH) differs from non-LH primarily in terms of etiology, i.e. cerebral amyloid angiopathy is the

Analyses of Mortality and Prevalence of Cerebrovascular Disease in Colombia, South America (2014-2016): A Cross-Sectional and Ecological Study.

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Stroke is the second cause of death and the first cause of disability worldwide. However, although numerous reports regarding stroke epidemiology in Latin America have been published, they differ widely in terms of employed methods and end points. This is the first of a series of

Prenatal high-fat diet alters the cerebrovasculature and clearance of β-amyloid in adult offspring.

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Alzheimer's disease (AD) is characterized by the accumulation of β-amyloid (Aβ) peptides in the extracellular spaces of the brain as plaques and in the walls of blood vessels as cerebral amyloid angiopathy (CAA). Failure of perivascular drainage of Aβ along cerebrovascular basement membranes

Chronic oral administration of adipoRon reverses cognitive impairments and ameliorates neuropathology in an Alzheimer's disease mouse model.

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Circulating adiponectin (APN) levels decrease with age and obesity. On the other hand, a reduction in APN levels is associated with neurodegeneration and neuroinflammation. We previously showed that aged adiponectin knockout (APN^-/-) mice developed Alzheimer's like pathologies, cerebral

Cerebral hypoperfusion and glucose hypometabolism: Key pathophysiological modulators promote neurodegeneration, cognitive impairment, and Alzheimer's disease.

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Aging, hypertension, diabetes, hypoxia/obstructive sleep apnea (OSA), obesity, vitamin B12/folate deficiency, depression, and traumatic brain injury synergistically promote diverse pathological mechanisms including cerebral hypoperfusion and glucose hypometabolism. These risk factors trigger

Vascular cognitive impairment: Modeling a critical neurologic disease in vitro and in vivo.

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Vascular contributions to cognitive impairment and dementia (VCID) is a complex form of dementia, combining aspects of vascular disease and other forms of dementia, such as Alzheimer's disease. VCID encompasses a wide spectrum of cerebrovascular-driven cognitive impairment, from mild cognitive

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