Journal of Alzheimer's disease : JAD
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Apolipoprotein E4 (ApoE4) has been considered to have detrimental effects on the age of onset and progression in Alzheimer's disease. Evidence continues to accumulate regarding the effects of ApoE isoforms in a number of other neurological diseases. ⋯ It further provides evidence of the effect neuroinflammation has in increasing susceptibility to cognitive decline in younger patients. Determining where these diverse diseases intersect and diverge in their relationship to ApoE provides insight into the two-hit mechanism in cognitive decline.
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Alzheimer's disease (AD) is a progressive, neurodegenerative disease characterized by an increasing incidence. One of the pathologic processes that underlie this disorder is impairment of brain microvasculature. ⋯ With transcranial ultrasound, the most frequently studied parameters are cerebral blood flow velocities and pulsatility indices, cerebrovascular reserve capacity, and cerebral microembolization. On the basis of current knowledge, we recommend using as a transcranial Doppler sonography screening method of choice the assessment of cerebrovascular reserve capacity with breath-holding test.
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Review
Influence of anesthetics on Alzheimer's disease: biophysical, animal model, and clinical reports.
Since the finding in the 1880 s that elderly patients may experience cognitive decline following surgery, the search for an understanding of this phenomenon has been underway. In the last decade, evidence from biophysical (light scattering and nuclear magnetic resonance), in vitro, in vivo animal studies, retrospective evaluations of human registries, and recently prospective randomized trials have explored the idea that various anesthetic agents play a role in this phenomenon by interacting with the biochemical mechanisms that are also responsible for the development of Alzheimer's disease. In the current review, we examine the evidence available and conclude that there is significant evidence to suggest an important role for this mechanism.
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Alzheimer's disease (AD) is a major social and clinical burden in the elderly, affecting 5% of people aged over 65 and 20% aged over 80. Despite improved management, a cure has not been found and hence analysis of predisposing factors to identify preventive strategies has become increasingly important. Surgery and anesthesia have been proposed to increase the incidence of post-operative cognitive decline (POCD) and AD. ⋯ Therapeutic success is, however, often not achieved, since these treatment methods do not address the ongoing neuroinflammatory processes and hence novel therapeutic and protective strategies are urgently needed. This review provides an insight into the current understanding of age-related cognitive impairment post-surgery and reflects on novel markers of AD pathogeneses exploring their use as targets for treatment. It gives a summary of recent efforts in preventing and treating POCD or AD with regards to the choice and depth of anesthesia, surgical strategy, and peri-operative medication, and discusses the mechanism of action and therapeutic prospects of novel agents.
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To date, the exact pathogenesis of dementia is still unknown. The most frequently hypothesized initiating factor is an accumulation of the protein amyloid-β in the brain, which has been associated with dementia of the Alzheimer type. Another potentially important initiating factor is a disrupted blood-brain barrier. ⋯ Although amyloid-β and blood-brain barrier dysfunction have both been associated with one particular type of dementia (Alzheimer's disease and vascular dementia, respectively), they co-exist in most demented patients. In fact, increasing evidence indicates that amyloid-β and blood-brain barrier disruption may interact and facilitate each other in their effect on neurodegeneration. The present systematic analysis describes the available evidence for a significant interplay between amyloid-β and blood-brain barrier function in dementia.