Dietary factors and Alzheimer’s disease
Taub Institute for Research of Alzheimer's Disease and the Aging Brain, Division of General Medicine, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, USA. The Lancet Neurology
(Impact Factor: 21.9).
11/2004; 3(10):579-87. DOI: 10.1016/S1474-4422(04)00878-6
Alzheimer's disease (AD) is increasing in prevalence, and environmental risk factors have not been identified with certainty. There is evidence that oxidative stress, homocysteine-related vitamins, fats, and alcohol have a role in the pathogenesis of AD. Few large epidemiological studies have explored the associations between nutrients and AD, and there has been only one trial of vitamin E in the prevention of AD. Some studies suggest that high intake of vitamins C, E, B6, and B12, and folate, unsaturated fatty acids, and fish are related to a low risk of AD, but reports are inconsistent. Modest to moderate alcohol intake, particularly wine, may be related to a low risk of AD. Available data do not permit definitive conclusions regarding diet and AD or specific recommendations on diet modification for the prevention of AD.
Available from: Emmanuel Dias-Neto
- "Cholinesterase inhibitors have shown symptomatic benefits in patients with mild to moderate AD, but to date there is no pharmacological treatment able to halt or slow the disease progression (Frisardi et al. 2010). There is growing evidence that nutrition plays an important role in the prevention of AD, and a great deal of attention has been paid to dietary fat and antioxidants (Butterfield et al. 2002; Luchsinger and Mayeux 2004). Most of the studies evaluating the potential benefits of dietary lipids on AD have focused on n-3 fatty acids. "
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ABSTRACT: Reduced phospholipase A2 (PLA2) activity has been reported in blood cells and in postmortem brains of patients with Alzheimer disease (AD), and there is evidence that conjugated linoleic acid (CLA) modulates the activity of PLA2 groups in non-brain tissues. As CLA isomers were shown to be actively incorporated and metabolized in the brains of rats, we hypothesized that feeding a diet naturally enriched in CLA would affect the activity and expression of Pla 2 -encoding genes in rat brain tissue, with possible implications for memory. To test this hypothesis, Wistar rats were trained for the inhibitory avoidance task and fed a commercial diet (control) or experimental diets containing either low CLA- or CLA-enriched butter for 4 weeks. After this period, the rats were tested for memory retrieval and killed for tissue collection. Hippocampal expression of 19 Pla 2 genes was evaluated by qPCR, and activities of PLA2 groups (cPLA2, iPLA2, and sPLA2) were determined by radioenzymatic assay. Rats fed the high CLA diet had increased hippocampal mRNA levels for specific PLA2 isoforms (iPla 2 g6γ; cPla 2 g4a, sPla 2 g3, sPla 2 g1b, and sPla 2 g12a) and higher enzymatic activity of all PLA2 groups as compared to those fed the control and the low CLA diet. The increment in PLA2 activities correlated significantly with memory enhancement, as assessed by increased latency in the step-down inhibitory avoidance task after 4 weeks of treatment (r s = 0.69 for iPLA2, P < 0.001; r s = 0.81 for cPLA2, P < 0.001; and r s = 0.69 for sPLA2, P < 0.001). In face of the previous reports showing reduced PLA2 activity in AD brains, the present findings suggest that dairy products enriched in cis-9, trans-11 CLA may be useful in the treatment of this disease.
Available from: Barbara Cardoso
- "Morris et al44 and Devore et al45 associated a higher intake of vitamin E but not vitamin C with a lower long-term risk of dementia over a mean follow-up period of 2 years and 9.6 years, respectively. Luchsinger and Mayeux46 found no relationship between the intake of vitamins C and E from food or supplements and the risk of developing AD during 4 years of follow-up time. In a cross-sectional study, Gu et al9 evaluated the association between nutrient intake and plasma Aβ levels in a cognitively healthy elderly population. "
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ABSTRACT: Alzheimer's disease (AD) is the most common form of dementia, and it generally affects the elderly. It has been suggested that diet is an intensively modifiable lifestyle factor that might reduce the risk of AD. Because epidemiological studies generally report the potential neuronal protective effects of various micronutrients, the aim of this study was to perform a literature review on the major nutrients that are related to AD, including selenium, vitamins C and E, transition metals, vitamin D, B-complex vitamins, and omega-3 fatty acids.
Available from: Dana M Niedowicz
- "Aβ accumulation in sporadic AD arises from an imbalance between its production and degradation, though the processes underlying this imbalance are unclear and likely intertwined. It is well-documented that lifestyle and overall health impact disease development and progression, however       . Leptin is a hormone released from adipose tissue that regulates satiety and energy balance via hypothalamic signaling in the brain and subsequent neuropeptide release . "
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ABSTRACT: Alzheimer's Disease (AD) is the most common age-related neurodegenerative disease, affecting an estimated 5.3 million people in the United States. While many factors likely contribute to AD progression, it is widely accepted that AD is driven by the accumulation of β-amyloid (Aβ), a small, fibrillogenic peptide generated by the sequential proteolysis of the amyloid precursor protein by the β- and γ-secretases. Though the underlying causes of Aβ accumulation in sporadic AD are myriad, it is clear that lifestyle and overall health play a significant role. The adipocyte-derived hormone leptin has varied systemic affects, including neuropeptide release and neuroprotection. A recent study by Lieb et al (2009) showed that individuals with low plasma leptin levels are at greater risk of developing AD, through unknown mechanisms. In this report, we show that plasma leptin is a strong negative predictor of Aβ levels in the mouse brain, supporting a protective role for the hormone in AD onset. We also show that the inhibition of Aβ accumulation is due to the downregulation of transcription of the γ-secretase components. On the other hand, β-secretase expression is either unchanged (BACE1) or increased (BACE2). Finally, we show that only presenilin 1 (PS1) is negatively correlated with plasma leptin at the protein level (p<0.0001). These data are intriguing and may highlight a role for leptin in regulating the onset of amyloid pathology and AD.
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