Controlled trial of N-acetylcysteine for patients with probable Alzheimer’s disease

Adair, John C.; Knoefel, Janice E.; Morgan, Nancy

doi:10.1212/wnl.57.8.1515

Cited by 206 publications

(132 citation statements)

References 10 publications

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“…Cocco et al [13] reported that old rats treated with NAC showed a slight brain-specific improvement of mitochondrial energy production efficiency, mostly with NAD-dependent substrates, together with a decrease in carbonyl protein content and an increase in the amount of protein thiols of brain cytosolic fraction when compared with untreated animals. Adair et al [1] performed a clinical trial where NAC or placebo was administered in a double-blind fashion to patients with probable AD. They observed that NAC has a positive effect on nearly every outcome measure, although significant differences were obtained only for a subset of cognitive tasks.…”

Section: Discussionmentioning

confidence: 99%

Lipoic Acid and N-acetyl Cysteine Decrease Mitochondrial-Related Oxidative Stress in Alzheimer Disease Patient Fibroblasts

Moreira

Harris

Zhu

et al. 2007

JAD

172

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Abstract. In this study, we evaluated the effect of lipoic acid (LA) and N -acetyl cysteine (NAC) on oxidative [4-hydroxy-2-nonenal, N ε -(carboxymethyl)lysine and heme oxygenase-1] and apoptotic (caspase 9 and Bax) markers in fibroblasts from patients with Alzheimer disease (AD) and age-matched and young controls. AD fibroblasts showed the highest levels of oxidative stress, and the antioxidants, lipoic acid (1 mM) and/or N -acetyl cysteine (100 µM) exerted a protective effect as evidenced by decreases in oxidative stress and apoptotic markers. Furthermore, we observed that the protective effect of LA and NAC was more pronounced when both agents were present simultaneously. AD-type changes could be generated in control fibroblasts using N -methylprotoporphyrin to inhibit cytochrome oxidase assembly indicating that the the oxidative damage observed was associated with mitochondrial dysfunction. The effects of N -methylprotoporphyrine were reversed or attenuated by both lipoic acid and N -acetyl cysteine. These data suggest mitochondria are important in oxidative damage that occurs in AD. As such, antioxidant therapies based on lipoic acid and N -acetyl cysteine supplementation may be promising.

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Section: Discussionmentioning

confidence: 99%

Lipoic Acid and N-acetyl Cysteine Decrease Mitochondrial-Related Oxidative Stress in Alzheimer Disease Patient Fibroblasts

Moreira

Harris

Zhu

et al. 2007

JAD

172

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“…NAC is also beneficial in a mouse model of ALS (Andreassen et al 2000). In a 6-month controlled clinical trial of NAC supplementation in Alzheimer's patients, there was a trend for measures of cognitive function to decline less rapidly on all tests employed, albeit significant differences were seen for only a subset of the cognitive tasks (Adair et al 2001).…”

Section: Supplemental Nac In Aging Humans and Rodents Provides Versatmentioning

confidence: 99%

An increased need for dietary cysteine in support of glutathione synthesis may underlie the increased risk for mortality associated with low protein intake in the elderly

McCarty

DiNicolantonio

2015

AGE

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Restricted dietary intakes of protein or essential amino acids tend to slow aging and boost lifespan in rodents, presumably because they downregulate IGF-I/ Akt/mTORC1 signaling that acts as a pacesetter for aging and promotes cancer induction. A recent analysis of the National Health and Nutrition Examination Survey (NHANES) III cohort has revealed that relatively low protein intakes in mid-life (under 10 % of calories) are indeed associated with decreased subsequent risk for mortality. However, in those over 65 at baseline, such low protein intakes were associated with increased risk for mortality. This finding accords well with other epidemiology correlating relatively high protein intakes with lower risk for loss of lean mass and bone density in the elderly.

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“…N-acetylcysteine (NAC) has some antioxidant properties, and a brief double-blind, placebocontrolled, randomized trial of NAC was undertaken in 43 probable AD patients [158]. Participants received placebo or 50 mg/kg/day of NAC in three diluted doses.…”

Section: Clinical Trials Of Antioxidantsmentioning

confidence: 99%

Free radical-mediated damage to brain in Alzheimer's disease and its transgenic mouse models

Sonnen¹,

Breitner²,

Lovell³

et al. 2008

Free Radical Biology and Medicine

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Controlled trial of N-acetylcysteine for patients with probable Alzheimer’s disease

Cited by 206 publications

References 10 publications

Lipoic Acid and N-acetyl Cysteine Decrease Mitochondrial-Related Oxidative Stress in Alzheimer Disease Patient Fibroblasts

Lipoic Acid and N-acetyl Cysteine Decrease Mitochondrial-Related Oxidative Stress in Alzheimer Disease Patient Fibroblasts

An increased need for dietary cysteine in support of glutathione synthesis may underlie the increased risk for mortality associated with low protein intake in the elderly

Free radical-mediated damage to brain in Alzheimer's disease and its transgenic mouse models

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