The role of free radicals in canine counterpart of senile dementia of the Alzheimer type

Skoumalová, Alice; Rofina, J; Schwippelová, Z; Gruys, E.; Wilhelm, J.

doi:10.1016/s0531-5565(03)00071-8

Cited by 85 publications

(69 citation statements)

References 58 publications

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“…In our preceding study we found increased level of LFP in erythrocytes of dogs with canine counterpart of AD compared to age-matched control animals. Besides the quantitative difference the fluorescent species differed also in their fluorescence spectra, which further confirmed the disease specific product (Skoumalova et al, 2003).…”

Section: Discussionsupporting

confidence: 54%

“…The presence of LFP in erythrocytes of dogs with canine counterpart of AD was previously found (Skoumalova et al, 2003). It implied the intention to extend this study to AD patients.…”

Section: Accepted Manuscriptmentioning

confidence: 58%

“…Due to their native fluorescence they can be easily detected and have been used as an indicator of free radical damage to lipids in various tissues and pathologies (Goldstein and McDonagh, 1976, Skoumalova et al, 2003, Vasankari et al, 1995, Vesela et al, 2002, Wihlmark et al, 1996, Wilhelm and Herget, 1999.…”

Section: Accepted Manuscriptmentioning

confidence: 99%

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The lipid peroxidation products as possible markers of Alzheimer's disease in blood

Skoumalová

Ivica

Santorova

et al. 2011

Experimental Gerontology

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International audienceOxidative stress, which is present in Alzheimer's disease (AD), results in the formation of various end-products of free radical reactions with proteins and lipids. At present there are no reliable diagnostic biomarkers of AD in the blood. Therefore, specific products of lipid peroxidation in the blood of AD patients were investigated. Lipophilic extracts of erythrocytes in the group of patients with AD (n=44) and age-matched controls (n=16) were studied. The end-products of lipid peroxidation, so called lipofuscin-like pigments (LFP), were analyzed by fluorescence spectroscopy. It was found that the level of these products is significantly increased in erythrocytes of AD patients compared to controls. LFP were furher separated by means of HPLC into individual fractions to study their composition in AD and controls. The specific fraction of LFP in AD patients, which was isolated, might represent a disease-specific product in the blood

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Section: Discussionsupporting

confidence: 54%

“…The presence of LFP in erythrocytes of dogs with canine counterpart of AD was previously found (Skoumalova et al, 2003). It implied the intention to extend this study to AD patients.…”

Section: Accepted Manuscriptmentioning

confidence: 58%

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The lipid peroxidation products as possible markers of Alzheimer's disease in blood

Skoumalová

Ivica

Santorova

et al. 2011

Experimental Gerontology

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“…Aged dogs show damage to protein carbonyl groups in the brain Skoumalova et al 2003), in parallel with a reduction in endogenous antioxidant enzymes, including glutamine synthetase and superoxide dismutase (Kiatipattanasakul et al 1997;Head et al 2002). Several studies report evidence of increased oxidative damage to lipids (Papaioannou et al 2001;Head et al 2002;Rofina et al 2004Rofina et al , 2006 and DNA/RNA (Rofina et al 2006) in the aged canine brain.…”

Section: Why Study Aging In Dogs?mentioning

confidence: 99%

Strategies for improving cognition with aging: insights from a longitudinal study of antioxidant and behavioral enrichment in canines

Christie

Opii

Head

2008

AGE

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Studies in humans suggest that lifestyle factors can have a beneficial impact on the risk for developing cognitive decline and dementia with age. There is growing evidence that maintaining a physically and intellectually active lifestyle can positively impact cognitive ability in older individuals. Dietary factors, such as the intake of antioxidants, may also prevent age-related cognitive decline. However, studies in humans are challenging; many variables cannot be controlled, making it difficult for researchers to determine the exact types and quantities of enrichment and dietary factors necessary for positive effects on cognition. Studies in animal models of human aging allow researchers to precisely control such variables, and can be used to assess the mechanisms and molecular pathways underlying any positive effects. Here we review the results of an intervention study using a canine model of human aging. The study was unique in that it compared the effects of dietary antioxidant supplementation alone and in combination with behavioral enrichment. We found that both interventions lead to improvements in cognitive ability in aged dogs; however, combining the treatments preserved cognition to a greater extent than either treatment alone. Overall, the results suggest that antioxidant supplementation and behavioral enrichment target separate yet complementary molecular pathways to improve cognition, and support the idea that combinations of treatments to improve cognition and slow brain aging will produce greater benefits than single interventions.

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“…In the initiation phase, stage II (or the soluble toxic oligomers) may reinforce the ongoing aging process, increasing the generation of free radicals [80] and leading to more severe neuronal dysfunction. As found in AD, oxidative stress may also be related to high Zn 2+ levels that inhibit APP ferroxidase activity [13].…”

Section: Amyloid Reactivitymentioning

confidence: 99%

Dogs with Cognitive Dysfunction Syndrome: A Natural Model of Alzheimer’s Disease

Bosch¹,

Pugliese²,

Gimeno-Bayón³

et al. 2012

CAR

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In the search for appropriate models for Alzheimer's disease (AD) involving animals other than rodents, several laboratories are working with animals that naturally develop cognitive dysfunction. Among the animals tested, dogs are quite unique in helping to elucidate the cascade of events that take place in brain amyloid-beta (Aβ) deposition aging, and cognitive deficit. Recent innovative research has validated human methods and tools for the analysis of canine neuropathology and has allowed the development of two different approaches to investigate dogs as natural models of AD. The first approach relates AD-like neuropathy with the decline in memory and learning ability in aged housed dogs in a highly controlled laboratory environment. The second approach involves research in family-owned animals with cognitive dysfunction syndrome. In this review, we compare the strengths and limitations of housed and family-owned canine models, and appraise their usefulness for deciphering the early mechanisms of AD and developing innovative therapies.KEYWORDS: aging, Amyloid-beta, animal model, canine cognitive dysfunction syndrome, family dog, therapies. 6 Why a canine model of AD?For years, the search for appropriate animal models for Alzheimer's disease (AD) has focused on a variety of manipulations to reproduce the disease in various species, such as yeast, Drosophyla melanogaster, Caenorabditis elegans, rodents, and rabbits, with a particular interest in obtaining knockout and transgenic animals (for a review, see [1]research is currently performed in the mouse because its brain structure is somewhat similar to that of humans, and it is amenable to highly sophisticated genetic engineering. Because age-related cognitive decline is a common feature of most mammals, other laboratories have focused on the few species that naturally develop cognitive dysfunction with various Alzheimer-like characteristics. These animals include the monkey, polar bear, cat and dog [2][3][4][5]. Canine models are currently considered a useful intermediate between genetically modified mouse models and humans [6,7]. Although many of the transgenic AD models have provided insights into the molecular mechanisms of the pathology, none of them encompass all the cognitive deficits observed in AD (see Table 1). One of the first transgenic mouse AD models was the amyloid precursor protein transgenic mouse, PDAPP mouse, which develops age-dependent amyloid beta accumulation and deposition in both diffuse and fibrillar neuritic plaques in the hippocampus, cerebral cortex, and corpus callosum [8]. Other models with AD-like pathology are apolipoprotein E (ApoE) or Tau transgenic mice, and also mice in which other genes have been modified. In more sophisticated approaches, important information has been gained from crossing PDAPP and ApoE models and with mice lacking or over-expressing genes for beta-secretase, alpha-secretase, or the insulin-degrading enzyme [9,10].All these models have provided valuable information on AD pathology and on the poss...

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The role of free radicals in canine counterpart of senile dementia of the Alzheimer type

Cited by 85 publications

References 58 publications

The lipid peroxidation products as possible markers of Alzheimer's disease in blood

The lipid peroxidation products as possible markers of Alzheimer's disease in blood

Strategies for improving cognition with aging: insights from a longitudinal study of antioxidant and behavioral enrichment in canines

Dogs with Cognitive Dysfunction Syndrome: A Natural Model of Alzheimer’s Disease

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