Relationship between Dementia and Nutrition-Related Factors and Disorders: An Overview

Salerno-Kennedy, Rossana; Cashman, Kevin D.

doi:10.1024/0300-9831.75.2.83

Cited by 37 publications

(23 citation statements)

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“…This possibility should not be surprising, given the accumulating evidence that the risk of developing AD can be influenced by many factors (Cupples et al, 2004) including newly discovered gene-gene interactions (Borroni et al, 2004;Bernardini et al, 2005;Dunckley et al, 2005;Lambert et al, 2005;Papassotiropoulos et al, 2005) and gene-race interactions (Green et al, 2002;Gureje et al, 2006), as well as interactions with other medical (Evans et al, 2004), and lifestyle/environmental factors (Mutter et al, 2004;Bird, 2005;Salerno-Kennedy and Cashman, 2005), all of which contribute to disease pathogenesis in poorly understood ways. More work is needed to understand the factors in family history that confer AD risk and their influence on brain structure and function.…”

Section: Discussionmentioning

confidence: 99%

The Influence of Alzheimer Disease Family History and Apolipoprotein E ε4 on Mesial Temporal Lobe Activation

Johnson¹,

Schmitz²,

Trivedi³

et al. 2006

J. Neurosci.

142

152

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First-degree family history of sporadic Alzheimer disease (AD) and the apolipoprotein E 4 (APOE4) are risk factors for developing AD. Although the role of APOE4 in AD pathogenesis has been well studied, family history remains a rarely studied and poorly understood risk factor. Both putatively cause early brain changes before symptomatic disease, but the relative contribution of each to brain function is unknown. We examined 68 middle-aged participants with a parent diagnosed with AD [family history (ϩFH)] and 64 age-and educationmatched controls without a first-degree family history of any dementia [no family history (ϪFH)]. All underwent cognitive testing, APOE genotyping, and a functional magnetic resonance imaging encoding task that required discrimination of novel items from previously learned items. A 2 ϫ 2 factorial ANOVA (presence/absence of parental family history and presence/absence of the APOE4) was used to detect group effects. A greater response to novel items was detected in the mesial temporal lobe and fusiform gyrus bilaterally among persons without a first-degree family history of AD. In hippocampal areas, the ϪFH ϩ4 group exhibited the greatest signal change, and the ϩFH ϩ4 group exhibited the least. These findings indicate that FH of AD is an important predictor of hippocampal activation during encoding and that FH may modulate the effect of APOE4 in these middle-aged adults, suggesting that an as yet unspecified factor embodied in first-degree family history of AD is influencing the expression of APOE4 on brain function.

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Section: Discussionmentioning

confidence: 99%

The Influence of Alzheimer Disease Family History and Apolipoprotein E ε4 on Mesial Temporal Lobe Activation

Johnson¹,

Schmitz²,

Trivedi³

et al. 2006

J. Neurosci.

142

152

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“…While a complete review of the effects of nutrition, diet, and physical activity on risk of dementia is beyond the scope of this paper, it is to be noted that both increased physical activity [63], and certain nutritional elements, such as unsaturated fats, vitamin C, E, B6, B12, and folate [64,65] are associated with a lower risk of dementia and AD. Conversely, diets high in saturated fat are found to increase risk of AD [66,67], and lead to impaired cognitive performance in animal models [68].…”

Section: Nutrition and Physical Activity As Mitigating Factorsmentioning

confidence: 97%

The Epidemiology of Adiposity and Dementia

Whitmer

2007

CAR

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Adipose tissue is the largest endocrine gland in the body, yet only recently has its role in neurodegenerative disease been considered. Prospective population level evidence has emerged to show that both obesity and overweight, is associated with an increased risk of all cause dementia, Alzheimer's disease (AD), and underlying neurodegenerative changes. Weight loss in late life however is associated with dementia, and those categorized as underweight are also at a greater risk of dementia. Given the current epidemic of obesity, and the expected age-related increase in dementia incidence, even a small association between these two diseases has far reaching public health implications. However, due to the effects of both AD-associated weight loss and age-related changes in body composition, there are methodological challenges in appropriately evaluating obesity as a risk factor for developing dementia. There is a need to take a 'life course approach' and to consider the role of risk factors prior to the onset of old age. Our work has shown that both obesity and overweight, as measured by body mass index and skinfold thickness, in middle-age are strongly associated with an increased risk of all cause dementia, Alzheimer disease & Vascular dementia, independent of the development of diabetes and cardiovascular-related morbidities. There is also value in assessing regional body shape distributions of adiposity, particular the role of abdominal obesity. Mechanistic pathways such as adipocyte secreted proteins and hormones, and inflammatory cytokines could explain the association between obesity and increased risk of dementia.

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“…In fact, bioactive compounds, such as antioxidants, mostly contained in fruits and vegetables, are important for the protection against oxidative and nitrosative stress, and these micronutrients have been related with aging itself and the pathophysiology of some age-related illnesses, including cognitive impairment and dementia [182]. While a growing body of knowledge demonstrates both the importance of oxidative stress in the etiology of dementia and the efficacy of antioxidant treatment in animal and cellular models, studies in humans are presently inconclusive [183,184]. In fact, epidemiological studies have demonstrated that dietary intake of natural or synthetic products with a putative antioxidant effect, mainly vitamin E, improve cognitive function and reduce the risk of AD [185,186].…”

Section: High Intakes Of Cereals Fruits and Vegetables In Admentioning

confidence: 99%

Diet and Alzheimer’s disease risk factors or prevention: the current evidence

Solfrizzi

Panza

Frisardi

et al. 2011

Expert Review of Neurotherapeutics

250

181

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Preventing or postponing the onset of Alzheimer's disease (AD) and delaying or slowing its progression would lead to a consequent improvement of health status and quality of life in older age. Elevated saturated fatty acids could have negative effects on age-related cognitive decline and mild cognitive impairment (MCI). Furthermore, at present, epidemiological evidence suggests a possible association between fish consumption, monounsaturated fatty acids and polyunsaturated fatty acids (PUFA; in particular, n-3 PUFA) and a reduced risk of cognitive decline and dementia. Poorer cognitive function and an increased risk of vascular dementia (VaD) were found to be associated with a lower consumption of milk or dairy products. However, the consumption of whole-fat dairy products may be associated with cognitive decline in the elderly. Light-to-moderate alcohol use may be associated with a reduced risk of incident dementia and AD, while for VaD, cognitive decline and predementia syndromes, the current evidence is only suggestive of a protective effect. The limited epidemiological evidence available on fruit and vegetable consumption and cognition generally supports a protective role of these macronutrients against cognitive decline, dementia and AD. Only recently, higher adherence to a Mediterranean-type diet was associated with decreased cognitive decline, although the Mediterranean diet (MeDi) combines several foods, micro- and macro-nutrients already separately proposed as potential protective factors against dementia and predementia syndromes. In fact, recent prospective studies provided evidence that higher adherence to a Mediterranean-type diet could be associated with slower cognitive decline, reduced risk of progression from MCI to AD, reduced risk of AD and a decreased all-cause mortality in AD patients. These findings suggested that adherence to the MeDi may affect not only the risk of AD, but also of predementia syndromes and their progression to overt dementia. Based on the current evidence concerning these factors, no definitive dietary recommendations are possible. However, following dietary advice for lowering the risk of cardiovascular and metabolic disorders, high levels of consumption of fats from fish, vegetable oils, nonstarchy vegetables, low glycemic index fruits and a diet low in foods with added sugars and with moderate wine intake should be encouraged. Hopefully this will open new opportunities for the prevention and management of dementia and AD.

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Relationship between Dementia and Nutrition-Related Factors and Disorders: An Overview

Cited by 37 publications

References 0 publications

The Influence of Alzheimer Disease Family History and Apolipoprotein E ε4 on Mesial Temporal Lobe Activation

The Influence of Alzheimer Disease Family History and Apolipoprotein E ε4 on Mesial Temporal Lobe Activation

The Epidemiology of Adiposity and Dementia

Diet and Alzheimer’s disease risk factors or prevention: the current evidence

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