Journal of Alzheimer's disease : JAD
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Recent studies have suggested that general anesthesia may initiate or accelerate cognitive impairment and Alzheimer's disease (AD). To understand the possible underlying mechanisms, several studies have been carried out in animal models. In this review, we first briefly discuss the mechanisms leading to neurodegeneration and cognitive impairment in AD, with an emphasis on tau abnormalities in this pathological process. ⋯ Recent studies suggest that anesthesia may accelerate the development of AD by promoting abnormal hyperphosphorylation of tau. Further studies are certainly needed to understand the molecular mechanism by which anesthesia may initiate or accelerate cognitive impairment and AD. An understanding of the mechanism will help develop strategies for preventing or eliminating this adverse effect of anesthesia.
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The evaluation and management of patients with cognitive decline pose many diagnostic and therapeutic challenges. While most cognitive disorders need a standard screening for common reversible causes, the diagnosis of `not so usual' causes are delayed and often missed. ⋯ Many more metabolic, nutritional, endocrinal, toxic, post operative, autoimmune, cerebrovascular, genetic, infectious, and hemorheological factors are now emerging as unusual causes. This review deals with the recognition and evaluation of these unusual causes of cognitive decline.
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Review
Postoperative cognitive dysfunction: toward the Alzheimer's disease pathomechanism hypothesis.
Alzheimer's disease (AD), a chronic and progressive deterioration of memory and other cognitive domains, is the most common form of dementia. Because of related health and social impact, there is growing interest in assessing potential relationship between anesthesia and the onset and progression of chronic neurodegenerative disorders, including AD. ⋯ Preclinical studies are providing an increasing body of evidences on some of the mechanisms that link anesthetics to neuronal programmed cell death (apoptosis) and accumulation of misfolded proteins in the aging brain. Therefore, risk factors and pathomechanisms of chronic neurodegenerative disorders, including AD, and persistent postoperative-postanesthesia cognitive dysfunction may overlap.
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Both short and long term cognitive changes occur after cardiac surgery but the pathophysiology of these neurobehavioral changes remain incompletely understood. The cause of cognitive decline is most likely multifactorial and probably represents a complex interaction between cerebral microemboli, global cerebral hypoperfusion, inflammation, and genetic susceptibility. The problem of cognitive decline after cardiac surgery continues to increase as the surgical population becomes older and has more prevalent comorbid diseases. A better understanding of the etiology is essential to finding new preventive strategies as no definitive therapy exists for cognitive dysfunction.
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With a growing aging population, more patients suffering from dementia are expected to undergo surgery, thus being exposed to either general or regional anesthesia. This calls for specific attention ranging from the legal aspects of obtaining informed consent in demented patients to deciding on the use of premedication, choice of anesthetics, and management of postoperative pain. This review reflects on both general considerations concerning geriatric patients but also on the specific features of perioperatively used drugs and anesthetics that might have an impact on patients with Alzheimer's disease (AD).