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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Review Meta Analysis
The impact of general and regional anesthesia on the incidence of post-operative cognitive dysfunction and post-operative delirium: a systematic review with meta-analysis.
Post-operative cognitive complications such as delirium have been consistently associated with poor short and long term outcomes, and the role of anesthesia, particularly the role of general versus regional anesthesia, remains unclear. The objective of this systematic review with meta-analysis was to compare the influence of general, regional, or a combination of anesthesia on the development of Post-Operative Cognitive Dysfunction (POCD) and Post-Operative Delirium (POD). Standard bibliographic databases were searched and complimented by hand searching of original and review article references. ⋯ In conclusion, it appears that general anesthesia, compared to others, may increase the risk of developing POCD; however this has not been shown for POD. Possible reasons for this finding have been explored. This data would advocate for the use of regional anesthesia wherever possible especially in people otherwise vulnerable to developing cognitive symptoms.
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Several studies conducted worldwide report an inverse association between caffeine/coffee consumption and the risk of developing Parkinson's disease (PD). However, heterogeneity and conflicting results between studies preclude a correct estimation of the strength of this association. We conducted a systematic review and meta-analysis of published epidemiological studies to better estimate the effect of caffeine exposure on the incidence of PD. ⋯ The negative association was weaker when only women were considered (RR=0.86, 95%CI: 0.73-1.02; I2=12.9%). A linear relation was observed between levels of exposure to caffeine and the RR estimates: RR of 0.76 (95%CI: 0.72-0.80; I2= 35.1%) per 300 mg increase in caffeine intake. This study confirm an inverse association between caffeine intake and the risk of PD, which can hardly by explained by bias or uncontrolled confounding.
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Increasing evidence indicates that patients develop post-operative cognitive decline (POCD) following surgery. POCD is characterized by transient short-term decline in cognitive ability evident in the early post-operative period. This initial decline might be associated with increased risk of a delayed cognitive decline associated with dementia 3 to 5 years post-surgery. ⋯ Inflammation and a maladaptive stress response might also contribute to the pathophysiology of this disorder. Future research needs to identify predisposing factors, and then strategies to protect against POCD and subsequent dementia. The field also needs to adopt a more rigorous approach to codifying the frequency and extent of early and delayed post-operative cognitive decline.
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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.