Effect of Vitamin E and Memantine on Functional Decline in Alzheimer Disease

Dysken, Maurice W.; Sano, Mary; Asthana, Sanjay; Vertrees, Julia E.; Pallaki, Muralidhar; Llorente, Maria D.; Love, Susan; Schellenberg, Gerard D.; McCarten, J. Riley; Malphurs, Julie; Prieto, Susana; Chen, Peijun; Loreck, David; Trapp, George A.; Bakshi, Rajbir; Mintzer, Jacobo; Heidebrink, Judith L.; Vidal-Cardona, Ana; Arroyo, Lillian M.; Cruz, Angel R.; Zachariah, Sally B.; Kowall, Neil W.; Chopra, Mohit P.; Craft, Suzanne; Thielke, Stephen; Turvey, Carolyn; Woodman, Catherine; Monnell, Kimberly A.; Gordon, Kimberly; Tomaska, Julie; Segal, Yoav; Peduzzi, Peter; Guarino, Peter

doi:10.1001/jama.2013.282834

Cited by 499 publications

(352 citation statements)

References 38 publications

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“…Some studies indicated negative effects of high-dose vitamin E on cognitive function and increased risk for mortality [142]. A more recent randomized trial of vitamin E in veterans showed a 19 % delay in clinical progression per year [120]. In addition to vitamins C and E, several other antioxidant vitamins, including vitamins A, B 12 , and D, have been investigated owing to their deficient levels in patients with AD [111,113].…”

Section: Oxidative Damage As a Therapeutic Targetmentioning

confidence: 99%

Targeting the Prodromal Stage of Alzheimer's Disease: Bioenergetic and Mitochondrial Opportunities

2015

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Alzheimer's disease (AD) has a complex and progressive neurodegenerative phenotype, with hypometabolism and impaired mitochondrial bioenergetics among the earliest pathogenic events. Bioenergetic deficits are well documented in preclinical models of mammalian aging and AD, emerge early in the prodromal phase of AD, and in those at risk for AD. This review discusses the importance of early therapeutic intervention during the prodromal stage that precedes irreversible degeneration in AD. Mechanisms of action for current mitochondrial and bioenergetic therapeutics for AD broadly fall into the following categories: 1) glucose metabolism and substrate supply; 2) mitochondrial enhancers to potentiate energy production; 3) antioxidants to scavenge reactive oxygen species and reduce oxidative damage; 4) candidates that target apoptotic and mitophagy pathways to either remove damaged mitochondria or prevent neuronal death. Thus far, mitochondrial therapeutic strategies have shown promise at the preclinical stage but have had little-to-no success in clinical trials. Lessons learned from preclinical and clinical therapeutic studies are discussed. Understanding the bioenergetic adaptations that occur during aging and AD led us to focus on a systems biology approach that targets the bioenergetic system rather than a single component of this system. Bioenergetic system-level therapeutics personalized to bioenergetic phenotype would target bioenergetic deficits across the prodromal and clinical stages to prevent and delay progression of AD.

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Section: Oxidative Damage As a Therapeutic Targetmentioning

confidence: 99%

Targeting the Prodromal Stage of Alzheimer's Disease: Bioenergetic and Mitochondrial Opportunities

2015

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“…For example, considering the numerous important functions of vitamin E in the body, a vitamin E deficiency can result in many different diseases, including spinocerebellar ataxia [5], ataxia [6], myoclonus-dystonia syndrome [7], and various other diseases [8][9][10]. Furthermore, vitamin E has also been shown to be effective against certain diseases, such as cardiovascular diseases [11], Alzheimer's disease [12], and nephropathy [13]. As a type of nephropathy, acute kidney injury (AKI) has a high morbidity and mortality rates in clinical investigations.…”

Section: Introductionmentioning

confidence: 99%

Protective effect of vitamin E against acute kidney injury

Liu

Feng

Wang

et al. 2015

BME

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Abstract. It has been well-known for many years now that vitamin E is an essential nutrient; however, some of the physiological functions of this vitamin are still far from being understood. In recent years, a series of preclinical and clinical studies proposed a protective role of vitamin E on acute kidney injury (AKI), which has a high morbidity rate and mortality rate in clinical investigations. Based on the benefits associated with vitamin E, such as strong antioxidant function, low toxicity, rare side-effects, and low cost, this therapy strategy has garnered an extensive amount of interest in the scientific community for the development of new therapy modes against AKI. In this review, a concise overview of the application of vitamin E in the treatment of AKI is provided as well as a summary of a series of published data regarding the combination therapy modes and detailed therapy mechanisms of vitamin E-based therapy against AKI. At present, there are critical points of this therapy mode that are still in need of further clarification, meaning the current understanding of the role of vitamin E in the treatment of AKI remains incomplete. However, the development of more reliable pharmacological or biotechnical strategies with vitamin E for the eventual treatment of patients with AKI may guide the next chapter of vitamin E research.

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“…The results showed that a dosage of 2,000 IU/d α-tocopherol significantly delayed the progression of AD symptoms in mild to moderate AD and decreased caregiver burden. Moreover, the authors found no safety concern associated with vitamin E supplementation compared to the control group [46].…”

Section: B Clinical Trials Concerning Vitamin E Supplementationmentioning

confidence: 89%

Alzheimer’s Disease: An Epidemiologic Disaster From Nutritional Perspective

Péter

2017

JNHFS

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and over was 5.1%. The estimated ratio of these two age groups in the 28 EU countries for 2040 is 17.9% and 9.9%, and for 2050 it is projected to be 17. 2% and 10.9%, respectively [3] (Figure 1).Based on the data available, LE during the 20 th century increased by more than 30 years. By the year 2040 more than a quarter of the Europeans will be older than 65 years and one in seven will be at least 75 years of age. More importantly, health expectancy on average is 8-11 years shorter than LE and loss of cognitive functions and increase in dementia are major contributors of disability and disease during these last couple years of life [4,5].Alzheimer's Disease (AD) is the most common cause of dementia in people aged 60 years or older, representing approximately 60-70% of all cases [6].Currently at least 35 million peopleare affected by AD worldwide and this number is expected to quadruple by the year 2050. Although mortality due to HIV, stroke and heart disease decreased between 2000 and 2013 by 52%, 23% and 14%, respectively, death cases related to AD increased by 71% within the same timeframe, making AD the fourth leading cause of death in developed countries [7].The prevalence of AD increases with age, for example the proportion of people with AD in the US in 2015 was estimated as follows: <65 years: 4%; 65-74 years: 15%; 75-84 years: 43%; 85+ years: 38% [7]. Definition of ADAlois Alzheimer identified the first case of AD in a 51 year old woman, whose brain autopsy showed plaques and tangles that characterize AD [8].AD is a degenerative brain disease of unknown origin, usually developing slowly during the late middle age or in old age and worsens with time. AD results in progressive memory loss, impaired thinking, disorientation, changes in personality and mood. These symptoms are leading to profound decline in AbstractAlzheimer disease (AD) is a progressive, multifactorial, untreatable neurodegenerative disease with worldwide increasing incidence and prevalence in the ageing societies. Besides pharmaceutical drug development there is also a need for alternative solutions for both prevention and treatment. The major objective of this article is to summarize the non-modifiable and some modifiable risk factors of AD, including nutrition and diet, and to discuss different aspects of AD prevention. Optimizing the nutritional status of the general population as a preventive measure may provide additional support to therapeutic concepts as they become available. Already several randomized controlled trials demonstrated promising results for certain nutrients to decrease the risk of developing AD and maintaining cognitive performance. Moreover, symptoms of AD such as neuroinflammation, glucose dysregulation, homocysteine accumulation and neuronal loss can be considerably influenced by nutrition. Thus, lifelong optimal supply of essential micro-and macronutrients may contribute to delay the onset of AD. However, currently the scientific evidence regarding the effects of nutrients on AD is incomplete and there are many...

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Effect of Vitamin E and Memantine on Functional Decline in Alzheimer Disease

Cited by 499 publications

References 38 publications

Targeting the Prodromal Stage of Alzheimer's Disease: Bioenergetic and Mitochondrial Opportunities

Targeting the Prodromal Stage of Alzheimer's Disease: Bioenergetic and Mitochondrial Opportunities

Protective effect of vitamin E against acute kidney injury

Alzheimer’s Disease: An Epidemiologic Disaster From Nutritional Perspective

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