دانلود مقاله ISI انگلیسی شماره 30766
عنوان فارسی مقاله

متابولیسم بیش از حد در یک مدل موش تراریخته سه گانه بیماری آلزایمر

کد مقاله سال انتشار مقاله انگلیسی ترجمه فارسی تعداد کلمات
30766 2012 7 صفحه PDF سفارش دهید محاسبه نشده
خرید مقاله
پس از پرداخت، فوراً می توانید مقاله را دانلود فرمایید.
عنوان انگلیسی
Hypermetabolism in a triple-transgenic mouse model of Alzheimer's disease
منبع

Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)

Journal : Neurobiology of Aging, Volume 33, Issue 1, January 2012, Pages 187–193

کلمات کلیدی
' بیماری آلزایمر - تعادل انرژی - هزینه انرژی - 3
پیش نمایش مقاله
پیش نمایش مقاله متابولیسم بیش از حد در یک مدل موش تراریخته سه گانه بیماری آلزایمر

چکیده انگلیسی

A common feature of Alzheimer's disease (AD) is weight loss, even though there is often an increase in food intake in AD patients. The reasons for this weight loss are unknown, but may be due to increased energy expenditure (metabolic rate) or a reduction in energy intake. This was investigated in the present study, using a triple-transgenic (3xTgAD) mouse model of AD. Two-month-old 3xTgAD mice displayed greater food intake (17%) and body weight (34%) but no difference in metabolic rate, as compared with nontransgenic controls (non-Tg). At 12 months of age, 3xTgAD mice still consumed more food (30%), but their body weight was significantly lower (15%) than non-Tg controls. This reduction in body weight was accompanied by a significant rise in metabolic rate, indicated by greater oxygen consumption (24%) and carbon dioxide production (29%); the effects were also observed in 18-month-old 3xTgAD mice. These data demonstrate for the first time the existence of a hypermetabolic state in an experimental model of AD, but whether this can explain the weight loss observed in AD patients remains to be determined.

مقدمه انگلیسی

Alzheimer's disease (AD) is an age-related neurodegenerative disorder characterized by a progressive decline in cognitive function that is associated with the presence of amyloid-beta (Aβ) plaques and neurofibrillary tangles. Although obesity in midlife has been identified as a risk-factor for AD, weight loss is a common feature of the disease, affecting 30%–40% of patients with mild to moderate AD (Gillette et al., 2007, Gillette-Guyonnet et al., 2000, Guerin et al., 2005 and White et al., 1996). This weight loss leads to poorer health outcomes, such as an increased risk of infections, falls and muscular atrophy, with a resultant reduction in quality of life and an increase in morbidity. The risk of weight loss increases with the severity and progression of AD, and is a predictor of mortality (White et al., 1998 and White et al., 2004). Prevention of this life-threatening weight loss in AD is therefore a major goal, but currently the mechanisms responsible are unknown. To lose lean or fat mass, energy intake must be lower than demand (expenditure and storage). However, food intake in people with AD is usually adequate or even increased (Burns et al., 1989, Keene and Hope, 1997a, Keene and Hope, 1997b, Niskanen et al., 1993, Smith et al., 1999 and Spindler et al., 1996). Weight loss can occur if energy expenditure (metabolic rate) is raised. It is uncertain whether abnormalities in metabolism exist in AD patients because no change, an increase, or a reduction in metabolism has been reported (Donaldson et al., 1996, Poehlman et al., 1997, Niskanen et al., 1993, Prentice et al., 1989, Wang et al., 1997 and Wolf-Klein et al., 1995). Although no direct measurements of metabolic rate in animal models of AD have been reported to date, the existence of a hypermetabolic state is supported indirectly by the finding that energy intake is elevated, but body weight is lower, in some transgenic mouse AD strains (Pugh et al., 2007 and Vloeberghs et al., 2008). Therefore, the aim of this study was to examine longitudinally body weight, food intake, and metabolic rate in a triple-transgenic (3xTgAD) mouse model of AD. These mice overexpress human amyloid precursor protein (APPSwe), presenilin-1 (PS-1M146V) and tauP301L, and develop progressive age-dependent cognitive deficits as well as Aβ plaque pathology and neurofibrillary tangles (Oddo et al., 2003).

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