Age-related changes in nutritional status can play an important role in brain functioning. Specific nutrient deficiencies in the elderly, including omega-3 fatty acids, B-vitamins, and antioxidants among others, may exacerbate pathological processes in the brain. Consequently, the potential of nutritional intervention to prevent or delay cognitive impairment and the development of Alzheimer's disease (AD) is a topic of growing scientific interest. This review summarizes epidemiological studies linking specific nutritional deficiencies to mild cognitive impairment (MCI), as well as completed and ongoing nutritional studies in prevention of MCI and AD. Processes that underlie AD pathogenesis include: membrane/synaptic degeneration, abnormal protein processing (amyloid-beta, tau), vascular risk factors (hypertension, hypercholesterolemia), inflammation, and oxidative stress. Consideration of mechanistic evidence to date suggests that several nutritional components can effectively counteract these processes, e.g., by promoting membrane formation and synaptogenesis, enhancing memory/behavior, improving endothelial function, and cerebrovascular health. The literature reinforces the need for early intervention in AD and suggests that multi-nutritional intervention, targeting multiple aspects of the neurodegenerative process during the earliest possible phase in the development of the disease, is likely to have the greatest therapeutic potential.
"In recent years, studies have focused on different nutritional approaches to benefit AD patients. More specifically, foods rich in ω-3 fatty acids like docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) (found abundantly in marine fish), vitamins, and diverse groups of secondary, polyphenolic plant metabolites have been shown to be effective against several AD pathologies (Stevenson and Hurst, 2007; Kamphuis and Scheltens, 2010; Kim et al., 2010; Willis et al., 2010). In the following sections, we will focus on the progress made with some of the most promising plant secondary metabolites such as curcumin and apigenin. "
[Show abstract][Hide abstract] ABSTRACT: Alzheimer's disease (AD) is a progressive neurodegenerative disorder, characterized by
deposition of amyloid beta, neurofibrillary tangles, astrogliosis and microgliosis, leading to
neuronal dysfunction and loss in the brain. Current treatments for AD primarily focus on
enhancement of cholinergic transmission. However, these treatments are only
symptomatic, and no disease-modifying drug is available for AD patients. This review will
provide an overview of the proven antioxidant, anti-inflammatory, anti-amyloidogenic,
neuroprotective, and cognition-enhancing effects of curcumin and apigenin and discuss
thepotential of these compounds for AD prevention and treatment. We suggest that these
compounds might delay the onset of AD or slow down its progression, and they should
enter clinical trials as soon as possible
Neural Regeneration Research 01/2015; · 0.22 Impact Factor
"Observational studies examining different dietary patterns with regard to the risk of developing AD revealed that diets rich in red meat, high-fat dairy products, butter, and refined sugar were associated with a higher AD risk, whereas diets rich in grains, vegetables, fruit, poultry, fish, and nuts decreased the risk   . More specifically, foods rich in ω-3 fatty acids, vitamins, and diverse groups of polyphenolic plant secondary metabolites have been shown to be effective against several AD pathologies, including abnormal Aβ processing, synaptic degeneration, oxidative stress, and inflammation, and slowed the progression of cognitive decline    . Extensive research has accumulated data over the last few decades on the efficacy in AD treatment utilising anti-amyloidogenic, anti-oxidative, and anti-inflammatory properties of naturally occurring substances like curcumin, catechins (from green tea), several fatty acids, and polyphenols (anthocyanins) for example found in blueberries   . "
[Show abstract][Hide abstract] ABSTRACT: Alzheimer's disease (AD) is a progressive neurodegenerative disorder, characterized by deposition of amyloid beta, neurofibrillary tangles, astrogliosis and microgliosis, leading to neuronal dysfunction and loss in the brain. Bio- and histochemical evidence suggests a pivotal role of central and peripheral inflammation in its aetiopathology, linked to the production of free radicals. Numerous epidemiological studies support that the long-term use of non-steroidal anti-inflammatory drugs is preventive against AD, but these medications do not slow down the progression of the disease in already diagnosed patients. There are a number of studies focusing on traditional herbal medicines and small molecules (usually plant secondary metabolites) as potential anti-inflammatory drugs, particulary in respect to cytokine suppression. For instance, ω-3 polyunsaturated fatty acids and a number of polyphenolic phytochemicals have been shown to be effective against inflammation in animal and cell models. Some of these plant secondary metabolites have also been shown to possess antioxidant, anti-inflammatory, anti-amyloidogenic, neuroprotective, and cognition-enhancing effects. This review will overview the the effects of catechins/proanthocyanidins from green tea, curcumin from turmeric, extracts enriched in bacosides from Brahmi, Ginkgo flavone glycosides, and ω-3 polyunsaturated fatty acids not only counteract one pathophysiological aspect of AD in numerous in vitro and in vivo studies of models of AD, but also ameliorate several of the above mentioned pathologies. The evidence suggests that increased consumption of these compounds might lead to a safe strategy to delay the onset of AD. The continuing investigation of the potential of these substances is necessary as they are promising to yield a possible remedy for this pervasive disease.
CNS & Neurological Disorders - Drug Targets (Formerly Current Drug Targets - CNS & Neurological Disorders) 09/2014; 13(7). DOI:10.2174/1871527313666140917110635 · 2.63 Impact Factor
"A recent review article emphasized the potential role of nutritional supplementation to prevent cognitive decline by counteracting deleterious neurodegenerative and pathological process. The literature reinforces the need for early intervention in AD and suggests that multi-nutritional intervention, targeting multiple aspects of the neurodegenerative process during the earliest possible phase in the development of the disease, is likely to have the greatest therapeutic potential (56). Therefore effective, nutrition-based approaches would be of great benefit due to a relatively low risk of side effects in a presymptomatic or prodromal stage, and benefit a relatively healthy population allied to the necessarily long exposure time (57). "
[Show abstract][Hide abstract] ABSTRACT: Alzheimer's disease (AD) is the leading cause of dementia, and the most prevalent neurodegenerative disease in the elderly. The prevalence of AD is predicted to rise as life expectancy grows across populations. The exact cause of this devastating disease is still unknown; however, it is an aging-related multi-factorial disorder, and growing evidence supports the contribution of modifiable environmental factors to unmodifiable factors such as gene and ageing itself. The recent advancement of methodologies and techniques for early diagnosis of AD facilitates the investigation of strategies to reduce the risk for AD progression in the earliest stages of the disease. Pharmacological attempts at curing, halting or modifying it have, by and large, been unsuccessful, and no breakthrough is seen in the near future. However, a lot of elements that seem to contribute to the disease such as risk factors have been identified, mainly from epidemiological and basic research studies. Many of these are amenable to lifestyle modification. Therefore, prevention in the preclinical stage is likely the most effective way to decrease the incidence of this age-associated dreadful neurodegenerative condition, and its associated burden for individuals and society. We provide an overview of modifiable risk factors for AD along with the supporting evidence.
Journal of Korean Medical Science 07/2014; 29(7):886-892. DOI:10.3346/jkms.2014.29.7.886 · 1.27 Impact Factor
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