همزیستی حمله ی خواب و بیماری آلزایمر
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی|
|30166||2015||2 صفحه PDF||4 صفحه WORD|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Neurobiology of Aging, Volume 33, Issue 7, July 2012, Pages 1318–1319
2. روش ها
5. قدردانی ها
پیوست. داده های کمکی
A recent publication suggested that hypocretin (Hcrt, orexin) may mediate the neuropathological process leading to Alzheimer's disease (AD) and that antagonism of hypocretin receptors decreases this process. Narcoleptics have an approximately 90% loss of Hcrt neurons and commensurate reductions in the levels of Hcrt in their cerebrospinal fluid beginning at disease onset, usually before the age of 30. If Hcrt mediates the disease process, narcoleptics should be protected against AD. We examined the postmortem neuropathology and clinical records of 12 sequentially encountered cases of human narcolepsy. We found that AD was present in 4 of these narcoleptics, a prevalence that is similar to that of the general population.
Kang and colleagues (Kang et al., 2009) recently reported that levels of amyloid-β in brain interstitial fluid are high during periods of wakefulness, suggesting that higher levels of neuronal activity during wakefulness may promote the development of AD. They also found that the wake-promoting neuropeptide Hcrt1 increases levels of amyloid-β, whereas an Hcrt antagonist reduces amyloid-β levels. If low Hcrt signaling reduces amyloid release, then people with narcolepsy, who have lost most of their Hcrt neurons (Blouin et al., 2005, Crocker et al., 2005, Peyron et al., 2000, Thannickal et al., 2000 and Thannickal et al., 2007), should have a lower risk of developing AD.
نتیجه گیری انگلیسی
We examined the brain of a 75-year male with narcolepsy with cataplexy since he was 12 and an 8 year history of AD. Neuropsychological testing was consistent with AD, MRI showed moderate cortical atrophy, and SPECT scan revealed hypoperfusion of the temporal and parietal lobes. He had 85% loss of the Hcrt neurons and extensive plaques and tangles in the hippocampus and frontal and temporal cortex (Braak Stage 5/6), findings consistent with narcolepsy and AD. In a review of all 11 other individuals ages 69 to 95 (mean age 83; 6 male, 6 female) with narcolepsy with cataplexy for whom we have neuropathologic material, we found that 3 others, a 75 year old male, a 79 year old male and a 94 year old female, had clinical histories of dementia and neuropathology consistent with AD—an overall prevalence of 33%, similar to that of the general population (Evans et al., 1989 and Hebert et al., 2003). All had amyloid deposition typical of AD (See supplementary data). This data set encompasses the majority of identified brains of narcoleptics in the literature (Blouin et al., 2005, Crocker et al., 2005, Honda et al., 2009 and Thannickal et al., 2000).