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WITHDRAWN: MicroRNA-125b can Target p38MAPK to Resolve Intermittent Hypoxia- Induced Dementia in Murine Models
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The article entitled, “MicroRNA-125b can Target p38MAPK to Resolve Intermittent Hypoxia-Induced Dementia in MurineModels” submitted in Current Neurovascular Research (CNR) by Dr. Xu Chen has been withdrawn from the journal in accordancewith BSP Editorial Policies.
Nocturnal Hypoxemia Is Associated with Altered Parahippocampal Functional Brain Connectivity in Older Adults at Risk for Dementia.
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Intermittent oxygen deficiency as the cause of dementia.
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It is well known that peroxidic materials can be expected to accumulate in simple molecules such as ethers or complex organic systems. Most such peroxides are stable at body temperature for long periods of time. However, when the supply of oxygen is depleted, certain metallic substances, e.g. iron,
Puerarin decreases hypoxia inducible factor-1 alpha in the hippocampus of vascular dementia rats.
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In this study, a rat vascular dementia model was established by permanent bilateral common carotid arterial occlusion. Rats were intraperitoneally injected with puerarin 3 days before modeling, for 45 successive days. Results demonstrated that in treated animals hippocampal structures were clear,
Demonstrating a reduced capacity for removal of fluid from cerebral white matter and hypoxia in areas of white matter hyperintensity associated with age and dementia
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White matter hyperintensities (WMH) occur in association with dementia but the aetiology is unclear. Here we test the hypothesis that there is a combination of impaired elimination of interstitial fluid from the white matter together with a degree of hypoxia in WMH. One of the mechanisms for the
Potential contribution of microRNA-125b targeting p38MAPK to relieving intermittent hypoxia-induced dementia of rat models.
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Allowing for the correlation between intermittent hypoxia and impaired cognition, we intended to figure out whether and how dementia-relevant biomolecules (e.g. miR-125b and p38MAPK) might participate in weakening of intelligence in the context of intermittent hypoxia. Within this investigation,
Neurotransmitter-related enzymes and indices of hypoxia in senile dementia and other abiotrophies.
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Fifty-six brains from middle-aged and elderly normal as well as demented subjects and patients with provisional clinical diagnosis of other neurological and psychiatric diseases were assessed histologically. On this basis the specimens were classified into 14 diagnostic groups. A survey of potential
Sleep-disordered breathing, hypoxia, and risk of mild cognitive impairment and dementia in older women.
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BACKGROUND
Sleep-disordered breathing (characterized by recurrent arousals from sleep and intermittent hypoxemia) is common among older adults. Cross-sectional studies have linked sleep-disordered breathing to poor cognition; however, it remains unclear whether sleep-disordered breathing precedes
Okadaic Acid and Hypoxia Induced Dementia Model of Alzheimer's Type in Rats.
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Alzheimer's disease (AD) is the most common cause of progressive decline of memory function in aged humans. To study about a disease mechanism and progression, animal models for the specific disease are needed. For AD, although highly valid animal models exist, none of the existing models
Ameliorative Effect of Trans-Sinapic Acid and its Protective Role in Cerebral Hypoxia in Aluminium Chloride Induced Dementia of Alzheimer's Type.
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BACKGROUND
Trans-Sinapic Acid is a bioactive compound. Recent studies showed that it has a significant potential to attenuate various chemically induced Neurodegenerative toxicities.
OBJECTIVE
The present study investigates the potential of trans-Sinapic Acid as neuromodulator and its effect on
Studies on the physiology of awareness; the correlation between intelligence and anoxemia in senile dementia.
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Dementia and hypoxia.
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Cerebral hypoxia and ischemia in the pathogenesis of dementia after stroke.
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Intermittent nocturnal hypoxemia in individuals with dementia: prevalence and relationship with functional status.
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[Ultrastructure of the cerebral cortex neurons in atherosclerotic dementia].
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Changes in neuron ultrastructure in the cortex of superior frontal and medial temporal gyri were studied in atherosclerotic dementia. Qualitative changes were shown to arise in cell organelles providing protein synthesizing and energy function along with quantitative ones. These changes as well as
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