Can Nutrients Prevent or Delay Onset of Alzheimer's Disease?

Kamphuis, Patrick; Scheltens, Philip

doi:10.3233/jad-2010-091558

Cited by 89 publications

(52 citation statements)

References 74 publications

(69 reference statements)

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“…The dietary changes include switching to either a ketogenic [53] or a Mediterranean diet [54] usually in addition to consuming various dietary supplements. The common dietary supplements include medium chain triglycerides; phosphatidylcholine and other membrane lipids; Moringa oleifera; turmeric; cocoa; niacin; and others [55]- [62]. A trusted colleague has told me that she has achieved consistent cognitive improvements in well over fifty elderly Alzheimer's patients during the last several years.…”

Section: Clinical Improvements In Alzheimer's Disease Patientsmentioning

confidence: 99%

“…Her therapies include the regular consumption of water containing sodium chloridedepleted minerals from the Great Salt Lake, other dietary supplements and having her patients adopt an optimistic, mindfulness, mental attitude. Most alternative medical practitioners are likely to attribute any apparent clinical benefits of dietary supplements either to an assumed anti-oxidant activity or to the correcting of supposed underlying nutrient or mineral deficiencies [62]. KELEA is absorbed by dipolar chemicals and it can be argued, that the reported beneficial dietary compounds act by increasing the supply of KELEA to the body [7].…”

Section: Clinical Improvements In Alzheimer's Disease Patientsmentioning

confidence: 99%

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Insufficiency of Cellular Energy (ICE) May Precede Neurodegeneration in Alzheimer’s Disease and Be Treatable via the Alternative Cellular Energy (ACE) Pathway

Martin¹

2017

AAD

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The term neurodegeneration emphasizes the destruction of neuronal cells as the primary explanation of many major neurological illnesses, including Alzheimer's disease. Specialized functioning of cells requires more cellular energy than is needed for basic cell survival. Cells can acquire energy both from the metabolism of food and from the alternative cellular energy (ACE) pathway. The ACE pathway is an added dynamic (kinetic) quality of the body's fluids occurring from the absorption of an external force termed KELEA (Kinetic Energy Limiting Electrostatic Attraction). KELEA is attracted to separated electrical charges and is seemingly partially released as the charges become more closely linked. As suggested elsewhere, the fluctuating electrical activity in the brain may attract KELEA from the environment and, thereby, contribute to the body's ACE pathway. Certain illnesses affecting the brain may impede this proposed antenna function of the brain, leading to a systemic insufficiency of cellular energy (ICE). Furthermore, individual neurons may derive some of the energy for their own activities from the repetitive depolarization of the cell. This may explain why hyper-excitability of neurons can occur in response to cell damage. This adaptive mechanism is unlikely to be sustainable, however, especially if there is a continuing need to synthesize neurotransmitters and membrane ion channels. The energy deficient neurons would then become quiescent and, although remaining viable, would not perform their intended specialized functions. Actual cell death would not necessarily occur till much later in the disease process. The distinction between quiescent and degenerated cells is important since the ACE pathway can be enhanced by several means, including the regular consumption of KELEA activated water. This, in turn, may improve the proposed antenna function of individual neurons, leading to a sustained restoration of specialized function via the ACE pathway. This paper

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Section: Clinical Improvements In Alzheimer's Disease Patientsmentioning

confidence: 99%

Section: Clinical Improvements In Alzheimer's Disease Patientsmentioning

confidence: 99%

Insufficiency of Cellular Energy (ICE) May Precede Neurodegeneration in Alzheimer’s Disease and Be Treatable via the Alternative Cellular Energy (ACE) Pathway

Martin¹

2017

AAD

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“…Evidence is mounting that alterations in dietary intake could be beneficial for preventing or treating AD (16,17). In recent years docosahexaenoic acid (DHA), an -3 polyunsaturated fatty acid predominantly found in marine fish and algae, has become of major interest.…”

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confidence: 99%

Docosahexaenoic Acid Reduces Amyloid β Production via Multiple Pleiotropic Mechanisms

Grimm

Kuchenbecker

Grösgen

et al. 2011

Journal of Biological Chemistry

195

150

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Alzheimer disease is characterized by accumulation of the ␤-amyloid peptide (A␤) generated by ␤-and ␥-secretase processing of the amyloid precursor protein (APP). The intake of the polyunsaturated fatty acid docosahexaenoic acid (DHA) has been associated with decreased amyloid deposition and a reduced risk in Alzheimer disease in several epidemiological trials; however, the exact underlying molecular mechanism remains to be elucidated. Here, we systematically investigate the effect of DHA on amyloidogenic and nonamyloidogenic APP processing and the potential cross-links to cholesterol metabolism in vivo and in vitro. DHA reduces amyloidogenic processing by decreasing ␤-and ␥-secretase activity, whereas the expression and protein levels of BACE1 and presenilin1 remain unchanged. In addition, DHA increases protein stability of ␣-secretase resulting in increased nonamyloidogenic processing. Besides the known effect of DHA to decrease cholesterol de novo synthesis, we found cholesterol distribution in plasma membrane to be altered. In the presence of DHA, cholesterol shifts from raft to non-raft domains, and this is accompanied by a shift in ␥-secretase activity and presenilin1 protein levels. Taken together, DHA directs amyloidogenic processing of APP toward nonamyloidogenic processing, effectively reducing A␤ release. DHA has a typical pleiotropic effect; DHA-mediated A␤ reduction is not the consequence of a single major mechanism but is the result of combined multiple effects.

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“…The omega-3 fatty acid docosahexaenoic acid (DHA), enriched in marine fish and algae, has been recently described to decrease Aβ generation in vitro and to decrease amyloid burden in animal models of AD [111][112][113][114][115][116][117] via pleiotropic mechanism, including a shift from amyloidogenic to non-amyloidogenic APP processing [73]. Alterations in dietary intake or functional foods might therefore be beneficial for preventing or treating AD [118][119][120].…”

Section: Non-amyloidogenic App Processingmentioning

confidence: 99%

Recent Understanding of the Molecular Mechanisms of Alzheimer?s Disease

Grimm¹,

Hartmann²

2011

J Addict Res Ther

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Alzheimer's disease (AD) is the most common form of dementia in the elderly and is characterized in patients by an inexorably progression, causing problems with memory, thinking and behaviour. Currently 25 million people worldwide are estimated to be affected by AD with the highest number in North America, Latin America, Western Europe, China and the western pacific [1]. Epidemiological studies predict that the incidence of AD will increase due to increasing life expectancy to 42.3 million in 2020 and 81.1 million in 2040 [1,2], emphasizing AD as a major public health concern.The two main histopathological hallmarks of AD are extracellular amyloid plaques and intracellular neurofibrillary tangles in vulnerable brain regions like hippocampus and cortex [3]. The amyloid plaques, also called senile plaques, are mainly composed of amyloid-beta peptides (Aβ), most of which are 38 to 43 amino acids long [4]. Aβ peptides are generated by sequential processing of the amyloid precursor protein (APP), a large type-I transmembrane protein [5] that belongs to an evolutionary conserved protein family including beside APP, the APP-like protein 1 (APLP1) and 2 (APLP2) in mammals [6,7] with the Aβ domain to be unique to APP [8]. The second characteristic pathological hallmark of AD, the intracellular neurofibrillary tangles, consist of an abnormally phosphorylated form of the microtubule-associated protein tau [9]. In contrast to amyloid plaques, which accumulate extracellularly in the brains of AD affected individuals and have been long believed to cause neuronal damage and cell death, neurofibrillary tangles are found inside neurons and their branching points like axons and dendrites [10,11]. Proteolytic Processing of APP Amyloidogenic APP processingProteolytic processing of APP leading to Aβ peptides is a ubiquitous cellular process involving β-and γ-secretase activity (Figure 1). The first step in Aβ production is APP cleavage by β-secretase, generating the N-terminus of Aβ. BACE 1 (β-site APP cleaving enzyme, also called Asp2 or memapsin2) was identified as the major β-secretase, a membrane-bound protease that belongs to the pepsin family of aspartyl proteases [12][13][14]. Aβ generation is abolished in cultures of BACE1-deficient embryonic cortical neurons [15] and in BACE1 knock-out mice [16,17]. Whereas Luo and Roberds et al. [16,17] reported a normal phenotype of BACE1-deficient mice, more recent studies found severe phenotypic abnormalities in BACE1 knock-out mice [18], challenging BACE1 as safe drug target for AD. Furthermore, additional BACE1 substrates have been reported, suggesting a variety of BACE1 physiological functions. Identified substrates include proteins with important neuronal function, like the β2-subunit of the voltage-gated sodium channel (Navβ2) [19,20], important for normal action potential regulation and neuronal excitability, and neuregulin-1 [21,22], as ligand for members of the ErbB family of receptor-tyrosine kinases, involved in synapse formation, myelination of central and peripheral axon...

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Can Nutrients Prevent or Delay Onset of Alzheimer's Disease?

Cited by 89 publications

References 74 publications

Insufficiency of Cellular Energy (ICE) May Precede Neurodegeneration in Alzheimer’s Disease and Be Treatable via the Alternative Cellular Energy (ACE) Pathway

Insufficiency of Cellular Energy (ICE) May Precede Neurodegeneration in Alzheimer’s Disease and Be Treatable via the Alternative Cellular Energy (ACE) Pathway

Docosahexaenoic Acid Reduces Amyloid β Production via Multiple Pleiotropic Mechanisms

Recent Understanding of the Molecular Mechanisms of Alzheimer?s Disease

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