Plasma antioxidants are similarly depleted in mild cognitive impairment and in Alzheimer’s disease

Rinaldi, Patrizia; Polidori, Maria Cristina; Metastasio, Antonio; Mariani, Elisabetta; Mattioli, Paola; Cherubini, Antonio; Catani, Marco; Cecchetti, Roberta; Senin, Umberto; Mecocci, Patrizia

doi:10.1016/s0197-4580(03)00031-9

Cited by 512 publications

(352 citation statements)

References 39 publications

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“…L and Z concentrations were positively related to premorbid cognitive function in the Georgia Centenarian Study (Johnson, 2012). Low serum concentrations of L and Z have been associated with AD and cognitive impairment (Kiko et al, 2012;Rinaldi et al, 2003) and also with AMD. AMD is the most common cause of blindness among the elderly in the western world and, interestingly, has been linked with an increased risk of dementia/cognitive impairment (Clemons et al, 2006;Klaver et al, 1999) and with a relative lack of MP (Beatty et al, 2001;Bone et al, 2001).…”

Section: Discussionmentioning

confidence: 95%

“…L and Z, together with cryptoxanthin, comprise ∼70% of carotenoids in the frontal and occipital cortices (Craft et al, 2004), and there are several lines of evidence suggesting a neuroprotective effect of L and Z in the brain. L supplementation has been shown to improve verbal fluency in older women , and plasma carotenoid levels have been associated with performance across a range of cognitive domains (Akbaraly et al, 2007) as well as being lower in individuals with mild cognitive impairment and Alzheimer's disease (AD) compared with normal controls (Rinaldi et al, 2003). Xanthophylls can attenuate the inflammatory effect of Aβ on the vasculature, thus potentially reducing the risk of AD (Nakagawa et al, 2011).…”

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confidence: 99%

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Low macular pigment optical density is associated with lower cognitive performance in a large, population-based sample of older adults

Feeney

Finucane

Savva

et al. 2013

Neurobiology of Aging

124

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Macular pigment (MP) is comprised of the carotenoids lutein (L), zeaxanthin (Z), and meso--zeaxanthin (MZ), which selectively accumulate at the macula (central retina) of the eye and are neuroprotective. These carotenoids are also present in the brain, and evidence suggests a close correlation between retinal and brain concentrations. We investigated the relationship between MP and cognitive function in 4453 adults aged ≥50 years as part of The Irish Longitudinal Study on Aging. Macular pigment optical density (MPOD) was determined using customized heterochromatic flicker photometry-a quick and noninvasive way of measuring the concentration of the pigment. Lower MPOD was associated with poorer performance on the mini--mental state examination (p = 0.026) and on the Montreal cognitive assessment (p = 0.016). Individuals with lower MPOD also had poorer prospective memory (p = 0.011), took longer time to complete a trail--making task (p = 0.003), and had slower and more variable reaction times on a choice reaction time task (p = 0.000 and 0.001). These associations were only slightly attenuated following adjustment for physical and mental health. There was no significant association between MPOD and verbal fluency, word recall, visual reasoning, or picture memory. Overall, the findings support the theory that xanthophyll carotenoids impact on cognitive function, underscoring the need for exploration of novel, noninvasive biomarkers for cognitive vulnerability and preventive strategies.

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Section: Discussionmentioning

confidence: 95%

mentioning

confidence: 99%

Low macular pigment optical density is associated with lower cognitive performance in a large, population-based sample of older adults

Feeney

Finucane

Savva

et al. 2013

Neurobiology of Aging

124

View full text Add to dashboard Cite

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“…Notably, similar increases in oxidative stress also occur systemically in AD. Lower plasma antioxidant levels and alterations in antioxidant enzyme activities are reported in mild cognitive impairment (MCI) patients and patients at early AD stages [19,[36][37][38][39] suggesting a systemic imbalance between ROS production and antioxidant defense systems in the plasma of AD patients and this is substantiated by increases in DNA, lipid, and protein oxidation products found in blood and cerebrospinal fluid (CSF) obtained from AD patients in comparison with controls [35,40,41]. Reflecting such a systemic oxidative imbalance in AD, we also found oxidative damage in olfactory neurons and the surrounding epithelial cells from AD donors [42], and another group reported increased 8-hydroxy-deoxyguanosine (8OHdG) in the DNA of lymphocytes from AD donors [43], which inversely correlated with the plasma levels of several antioxidant carotenoids [44].…”

Section: Vascular Oxidative Stress In Alzheimer Diseasementioning

confidence: 99%

Vascular oxidative stress in Alzheimer disease

Zhu

Smith

Honda

et al. 2007

Journal of the Neurological Sciences

160

156

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Alzheimer disease and cerebrovascular dementia are two common causes of dementia and, by present diagnostic criteria, are mutually exclusive using vascular pathology as an arbitrary demarcation in differential diagnosis. However, evidence from epidemiological, neuropathological, clinical, pharmacological, and functional studies suggest considerable overlap in risk factors and pathological changes suggesting shared common pathogenic mechanisms between these two diseases such that vascular factors play a vital role in the pathogenesis of Alzheimer disease. A high energy demand and lack of an endogenous fuel reserve make the brain highly dependent upon a continuous blood supply where disruption of cerebral blood vessels and blood flow can have serious consequences on neural activities. Indeed, many studies implicate metabolic defects in Alzheimer disease, such a reduced brain metabolism is one of the best documented abnormalities in the disease. Notably, since endothelial reactive oxygen species such as nitric oxide act as vasodilators at low concentrations, increased production coupled with elevated reactive oxygen species scavenging of nitric oxide, can lead to reduced bioavailability of nitric oxide and increased oxidative stress that damage sensitive vascular cells. In this respect, we and others have demonstrated that oxidative stress is one of the earliest pathological changes in the brain of Alzheimer disease patients and plays a critical role in the vascular abnormalities underlying metabolic defects in Alzheimer disease. Here, we discuss vascular factors in relation to Alzheimer disease and review hypoperfusion as a potential cause by triggering mitochondrial dysfunction and increased oxidative stress initiating the pathogenic process. KeywordsAlzheimer disease; hypoperfusion; mitochondria; nitric oxide; nitric oxide synthase; oxidative stress; vascular abnormalitiesCorrespondence to: George Perry, Ph.D., College of Sciences, University of Texas at San Antonio, 6900 North Loop 1604 West, San Antonio, Texas 78249-0661 USA, , george.perry@utsa.edu. 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. . Therefore, perivascular Aβ deposits may be a risk factor for reduced regional CBF [7]. Ultrastructural studies on blood vessels associated with Aβ deposits have shown their intermittent association with membrane abnormalities of smooth muscle cells [5]. Indeed, in AD cases with a clinical history of cerebral bleeding, the muscle layer is sometimes completely replaced by Aβ deposits, suggesting that the vascular system may be an initiator for the development of diseas...

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“…In the absence of an adequate antioxidant defense system, ROS and RNS damage to body lipids, nucleic acids and proteins has been consistently shown to be associated with the presence of AD-related alterations and symptoms as well as to disease severity. By-products of oxidative stress and redox unbalanced regulation as well as antioxidant depletion independent of diet have been repeatedly observed in plasma and tissues of patients with cognitive impairment even long prior to overt dementia manifestation (Praticó et al 2002;Rinaldi et al 2003) suggesting chronological primacy of oxidative stress in AD (Smith et al 2005;Yan et al 2013). The involvement of oxidative stress at different levels in AD in neuronal mitochondria is particularly deleterious due to their susceptibility to oxidative damage.…”

Section: Why Do We Need To Care About Dementiamentioning

confidence: 99%

Nutritional contributions to dementia prevention: main issues on antioxidant micronutrients

Polidori

Schulz

2014

Genes Nutr

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There is an impressing body of evidence supporting the beneficial role of balanced nutrition in lowering the risk of dementia and its commonest form, Alzheimer's disease. Nevertheless, and despite worldwide dementia epidemic, there is much unfounded skepticism and lack of information among physicians. As a result, the diagnosis of cognitive impairment occurs still far too late, at best symptomatic drugs keep being prescribed and patients and caregivers are left with little concrete support in the hands of the natural history of the disease. This review summarizes knowledge about the impact of nutrition as part of a healthy lifestyle and of micronutrients in particular on delaying and avoiding dementia onset.Why do we need to care about dementia Dementia is the most prevalent neurodegenerative disorder, and it is characterized by progression, multiple etiology, complex symptomatology including that related to a disturbance of cognitive performance and absence of a cure. During the course of the disease, the cognitive symptoms of dementia persist and steadily worsen and behavioral disturbances appear and progress and as a result intellectual and social abilities are affected enough to obstacle the performance of activities of daily living. According to dementia definition, a diagnosis of dementia can be done when the impairment of more cognitive domains lasts long enough and is associated with behavioral disturbances both affecting activities of daily living. Dementia is indeed associated with disability and a high grade of dependence on caregivers-usually family members. This condition of disability and dependence brings along an enormous social and economic burden which is linked to the epidemics of dementia and its commonest, untreatable form, Alzheimer's disease (AD). The major risk factor for dementia and AD is advanced age, and therefore, the societal impact of AD is increasing according to aging demographics (http:// ec.europa.eu/health/reports/european). Life expectancy at birth in the EU increased from 72 years in 1980 to 78 years in 2007. The population of industrialized countries progressed from a mean life expectancy of 35 years at the beginning of the last century, to currently over 80 years of age. People aged 65 years or older are expected to double between 1995 and 2050 to reach 135 million in the EU, with very old people, aged 80 years and older, being projected to grow as much as eight to ten times on the global scale by 2050. This will strongly impact the already challenging number of ten million AD cases in the EU. As a cure against dementia has not been found yet, health care professionals all over the world are predicted to face the diagnostic, therapeutic and socioeconomical challenges of over 115 million people with dementia by 2050 (Prince et al. 2013). This perspective might be even underestimated, particularly due to inadequate diagnosis, lack of awareness and low education. The dramatic loss of synapses and cholinergic neurons, accumulation of extracellular b amyloid (Ab) plaqu...

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Plasma antioxidants are similarly depleted in mild cognitive impairment and in Alzheimer’s disease

Cited by 512 publications

References 39 publications

Low macular pigment optical density is associated with lower cognitive performance in a large, population-based sample of older adults

Low macular pigment optical density is associated with lower cognitive performance in a large, population-based sample of older adults

Vascular oxidative stress in Alzheimer disease

Nutritional contributions to dementia prevention: main issues on antioxidant micronutrients

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