Link between heart disease, cholesterol, and Alzheimer's disease: A review

Sparks, D. Larry; Martin, Timothy A.; Gross, David R.; Hunsaker, John C.

doi:10.1002/1097-0029(20000815)50:4<287::aid-jemt7>3.0.co;2-l

Cited by 125 publications

(61 citation statements)

References 29 publications

(30 reference statements)

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“…When OE was added into already digested A␤ samples with trypsin ( Similarly, ESI-MS analysis of the A␤-OE Glu-C digest yielded signals corresponding to the expected A␤ fragments [4 -11], [12][13][14][15][16][17][18][19][20][21][22], and [23][24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40] following cleavage at the carboxy-terminus of glutamic acid (E) residues (Table 2), and the noncovalent complexes between OE and the [4 -11] and [12][13][14][15][16][17][18][19][20][21][22] A␤ Glu-C fragments ( Figure 3). Interactions between OE and the partially cleaved peptide fragments [4 -40] and (Table 4) When OE was added into already digested A␤ samples with Glu-C (Table 4), ESI signals corresponded to ...…”

Section: Resultsmentioning

confidence: 99%

“…Free radical reactions and oxidative stress [28,29], as well as unregulated immune response [30,31], are believed to be key factors for the pathogenesis of AD, whereas recent reports suggested a link between heart disease, hypercholesterolemia, and AD [32,33]. Thus, the well-documented antioxidant, anti-inflammatory, and antiatherogenic properties of OE may offer a multistage approach against the diverse mechanisms, which are inherent to AD.…”

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confidence: 99%

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Localization of the noncovalent binding site between amyloid-β-peptide and oleuropein using electrospray ionization FT-ICR mass spectrometry

Bazoti

Bergquist

Markides

et al. 2008

J. Am. Soc. Mass Spectrom.

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Abnormal accumulation and aggregation of amyloid-␤-peptide (A␤) eventually lead to the formation and cerebral deposition of amyloid plaques, the major pathological hallmark in Alzheimer's disease (AD). Oleuropein (OE), an Olea europaea L. derived polyphenol, exhibits a broad range of pharmacological properties, such as antioxidant, anti-inflammatory, and antiatherogenic, which could serve as combative mechanisms against several reported pathways involved in the pathophysiology of AD. The reported noncovalent interaction between A␤ and OE could imply a potential antiamyloidogenic role of the latter on the former via stabilization of its structure and prevention of the adaptation of a toxic ␤-sheet conformation. The established ␤-sheet conformation of the A␤ hydrophobic carboxy-terminal region and the dependence of its toxicity and aggregational propensity on its secondary structure make the determination of the binding site between A␤ and OE highly important for assessing the role of the interaction. In this study, two different proteolytic digestion protocols, in conjunction with high-sensitivity electrospray ionization mass spectrometric analysis of the resulting peptide fragments, were used to determine the noncovalent binding site of OE on A␤ and revealed the critical regions for the interaction. and its aggregational properties depend on both the peptide concentration and conformation, as well as on the solution conditions and pH [2,3]. It has been reported that reduction of the A␤ production, by controlling the cleavage of the larger transmembrane amyloid precursor protein (APP), or inhibition of its aggregation by using small molecules, which may interact noncovalently with A␤ and stabilize its structure, could serve as preventive or therapeutic approaches against AD [4]. In general, interruption of noncovalent interactions between protein and peptides, or even more between proteins/peptides and ligands can cause abnormalities, which often lead to diseases [5]. One interaction of this kind has been established between the Olea europaea derived bioactive compound, oleuropein (OE), and A␤ by means of electrospray ionization mass spectrometry (ESI-MS) [6]. This interaction could prove potent in inhibiting its aggregation.OE is a polyphenol extracted from the fruits and leaves of Olea europaea L. and possesses a wide range of pharmacological properties, such as antioxidant [7][8][9], anti-inflammatory [10, 11], antiatherogenic [12-14], antibacterial [15][16][17], and anticancer [18,19]. Moreover, OE and its metabolites have been shown to be potent against contemporary diseases, such as HIV [20,21] and osteoporosis [22,23]. Interestingly, in vitro [24] and epidemiological [25] studies demonstrated the positive impact of polyphenols on the onset of age-related disorders, such as dementia [26,27].It is regarded that the pathophysiology of AD is tangled and many theories have been proposed to illumine its mechanism. Free radical reactions and oxidative stress [28,29], as well as unregulated immune response [30,3...

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

Localization of the noncovalent binding site between amyloid-β-peptide and oleuropein using electrospray ionization FT-ICR mass spectrometry

Bazoti

Bergquist

Markides

et al. 2008

J. Am. Soc. Mass Spectrom.

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“…Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Sparks, 1997;Sparks, Martin, Gross, & Hunsaker III, 2000;Zatta, Zambenedetti, Stella, & Licastro, 2002). Based on the observation that patients with heart disease had beta amyloid staining in the brain (Sparks, 1999;Streit & Sparks, 1997), Sparks found that rabbits fed cholesterol to induce heart disease also had beta amyloid staining in the brain (Sparks et al, 1994;Sparks, 1997).…”

Section: Cholesterol Enhances Rabbit Heart Rate Conditioningmentioning

confidence: 99%

Cholesterol enhances classical conditioning of the rabbit heart rate response

Schreurs

Smith-Bell

Darwish

et al. 2007

Behavioural Brain Research

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The cholesterol-fed rabbit is a model of atherosclerosis and has been proposed as an animal model of Alzheimer's disease. Feeding rabbits cholesterol has been shown to increase the number of beta amyloid immunoreactive neurons in the cortex. Addition of copper to the drinking water of cholesterol-fed rabbits can increase this number still further and may lead to plaque-like structures. Classical conditioning of the nictitating membrane response in cholesterol-fed rabbits is retarded in the presence of these plaque-like structures but may be facilitated in their absence. In a factorial design, rabbits fed 2% cholesterol or a normal diet (0% cholesterol) for 8 weeks with or without copper added to the drinking water were given trace classical conditioning using a tone and periorbital electrodermal stimulation to study the effects of cholesterol and copper on classical conditioning of heart rate and the nictitating membrane response. Cholesterol-fed rabbits showed significant facilitation of heart rate conditioning and conditioning-specific modification of heart rate relative to normal diet controls. Consistent with previous research, cholesterol had minimal effects on classical conditioning of the nictitating membrane response when periorbital electrodermal stimulation was used as the unconditioned stimulus. Immunohistochemical analysis showed a significant increase in the number of beta amyloid positive neurons in the cortex, hippocampus and amygdala of the cholesterol-fed rabbits. Supplementation of drinking water with copper increased the number of beta amyloid positive neurons in the cortex of cholesterol-fed rabbits but did not produce plaque-like structures or have a significant effect on heart rate conditioning. The data provide additional support for our finding that, in the absence of plaques, dietary cholesterol may facilitate learning and memory. Cholesterol enhances rabbit heart rate conditioningThe cholesterol-fed rabbit has been used as an animal model of atherosclerosis since 1913 when Anitchkow first demonstrated that a cholesterol diet induced vascular lesions (Bocan, 1998;Fan & Watanabe, 2000;Finking & Hanke, 1997;Moghadasian, 2002). More recently, the cholesterol-fed rabbit has been proposed as an animal model of Alzheimer's disease (Ghribi, Larsen, Schrag, & Herman, 2006;Sjogren, Mielke, Gustafson, Zandi, & Skoog, 2006 Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Sparks, 1997;Sparks, Martin, Gross, & Hunsaker III, 2000;Zatta, Zambenedetti, Stella, & Licastro, 2002). Based on the observation that patients with heart disease had beta amyloid st...

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“…The significant chronic up-regulation of genes in the Alzheimer's disease pathway is particularly interesting as Alzheimer's disease plaques and heart disease have been shown in clinical studies co-occur (Sparks et al 2000). Heart disease and hypertension may be a forerunner to Alzheimer's disease, and Alzheimer's disease-like b-amyloid plaques have been found in the brains of non-demented individuals with heart disease (Sparks et al 2000).…”

Section: Extracting Meaning Using Go-term Meta-analysismentioning

confidence: 99%

“…Heart disease and hypertension may be a forerunner to Alzheimer's disease, and Alzheimer's disease-like b-amyloid plaques have been found in the brains of non-demented individuals with heart disease (Sparks et al 2000). Furthermore, cardiac amyloidosis is known to cause restrictive cardiomyopathy (Artz & Wynne 2000), a particularly lethal form of cardiomyopathy that does not respond to standard treatments.…”

Section: Extracting Meaning Using Go-term Meta-analysismentioning

confidence: 99%

From ‘omes to biology

Quackenbush

2006

Animal Genetics

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SummaryTechnologies that have emerged from the genome project have dramatically increased our ability to generate data on the way in which organisms respond to their environments, how they execute their programmes of development and growth, and how these are altered in the development of disease states. However, our ability to analyse these large datasets has not kept pace with our ability to generate them and consequently new strategies must be developed to address the issues associated with their analysis. One approach that we have employed quite successfully is to look at data from microarrays (or proteomics or metabolomics experiments) not as independent datasets, but rather as elements of a much larger body of biological information across various scales that must be integrated with, and interpreted within, the context of such ancillary data. Here we outline the general approach and provide three examples from published studies of the way in which we have applied this strategy.

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Link between heart disease, cholesterol, and Alzheimer's disease: A review

Cited by 125 publications

References 29 publications

Localization of the noncovalent binding site between amyloid-β-peptide and oleuropein using electrospray ionization FT-ICR mass spectrometry

Localization of the noncovalent binding site between amyloid-β-peptide and oleuropein using electrospray ionization FT-ICR mass spectrometry

Cholesterol enhances classical conditioning of the rabbit heart rate response

From ‘omes to biology

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