Mitochondrial aldehyde dehydrogenase polymorphism is not associated with incidence of Alzheimer's disease

Shin, In Sik; Stewart, Robert; Kim, Jae-Min; Kim, Sung‐Wan; Yang, Su-Jin; Shin, Hee‐Young; Jung, Jae Sung; Yoon, Jin‐Sang

doi:10.1002/gps.1401

Cited by 23 publications

(15 citation statements)

References 22 publications

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“…But the subsequent studies in Koreans didn't get the similar results [13,14]. To our knowledge, there has not been any association analysis of ALDH2 1/2 polymorphism with LOAD reported in Chinese.…”

Section: Introductioncontrasting

confidence: 62%

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The association of mitochondrial aldehyde dehydrogenase gene (ALDH2) polymorphism with susceptibility to late-onset Alzheimer's disease in Chinese

Wang

Zhou

et al. 2008

Journal of the Neurological Sciences

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Section: Introductioncontrasting

confidence: 62%

“…But the association studies from Korea failed to establish the statistically significant association between the ALDH2 1/ 2 polymorphism and AD progression [13,14]. These paradox findings may be due to ethnic differences of samples studied.…”

Section: Discussionmentioning

confidence: 89%

The association of mitochondrial aldehyde dehydrogenase gene (ALDH2) polymorphism with susceptibility to late-onset Alzheimer's disease in Chinese

Wang

Zhou

et al. 2008

Journal of the Neurological Sciences

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“…An association with late-onset AD (LOAD), interacting synergistically with the presence of the apolipoprotein E allele 4 (APOE ε4) has been detected in Japanese and Chinese subjects, whilst it was not reported in a population of Koreans [20][21][22][23][24]. A longitudinal study found that the incidence of AD in healthy participants was not correlated with ALDH polymorphism within 2.4 years [24]. In the mouse model, it has been shown that a deficiency in mitochondrial ALDH2 leads to age dependent memory impairment and increased lipid peroxidation [25].…”

mentioning

confidence: 99%

Increased Mitochondrial Aldehydedehydrogenase in the putamen of individuals with Alzheimer's disease

Michel

Gsell

Käsbauer

et al. 2010

JAD

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For decades, it has been acknowledged that oxidative stress due to free radical species contributes to the pathophysiology of aging and neurodegenerative diseases. Aldehyde dehydrogenases (ALDH) not only transform aldehydes to acids but also act as antioxidant enzymes. However, little is known about the implications of the enzymatic family of ALDH in the context of neurodegenerative processes such as Alzheimer's disease (AD). We therefore examined the enzymatic activity of the mitochondrial ALDH-isoform in different regions of the postmortem brain tissue isolated from patients with AD and controls. We found that the mitochondrial ALDH activity was significantly increased only in the putamen of patients suffering from AD compared to controls. This is of particular interest since mediators of oxidative stress, such as iron, are increased in the putamen of patients with AD. This study adds to the body of evidence that suggests that oxidative stress as well as aldehyde toxicity play a role in AD.

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“…Past studies on ALDH2 have focused on its relation to general cognitive function in patients with Alzheimer's disease (AD), Parkinson's disease (PD), and substance use disorders. Some studies proposed that ALDH2 A allele may be a risk factor of AD [22][23][24], but others disagreed [25][26][27][28]. Of the studies listed above, only Kim et al and Shin et al evaluated the general cognitive function of AD patients, but both of them failed to find a relation between general cognitive function and ALDH2 [25,26].…”

Section: Introductionmentioning

confidence: 99%

“…Some studies proposed that ALDH2 A allele may be a risk factor of AD [22][23][24], but others disagreed [25][26][27][28]. Of the studies listed above, only Kim et al and Shin et al evaluated the general cognitive function of AD patients, but both of them failed to find a relation between general cognitive function and ALDH2 [25,26]. Previous studies on ALDH2 and PD have focused on catecholaldehyde hypothesis, which suggested that ALDH2 inactivity may mediate the extent of damage to the dopamine system due to increased levels of toxic aldehydes [13].…”

Section: Introductionmentioning

confidence: 99%

Effect of Aldehyde Dehydrogenase 2 Gene Polymorphism on Executive Function in Opiate User

Liu¹,

Chen²,

Lu³

et al. 2018

Neuropsychiatry

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Objective: The use of opiate substances, such as heroin and methadone, has been proven to cause executive function damage. The extent of damage may be mediated by the activity of enzyme aldehyde dehydrogenase 2 (ALDH2), which plays an important role in neurotransmitter dopamine metabolism. The single nucleotide polymorphism Glu487Lys distributes mostly in Asia and codes for ALDH2 with greatly reduced enzyme activity. The current study aims to explore the effect of ALDH2 on executive function in opiate users. Methods: A total of 94 opiate users were recruited and 58 patients finished the neuropsychological assessment and blood genotyping. Results: After co-variating the influence of age and the years of education, we found that participants with ALDH2 A allele performed worse on the Category Complete index of the Modified Wisconsin Card Sorting Test (F = 5.34, p = 0.02), suggesting an impaired planning ability in this group. We also found that ALDH2 A carriers went through the Trail 2 in Color Trails Test faster (F = 8.21, p = 0.01), in part suggesting better set-shifting abilities; however, impulsiveness and lack of planning associated with this study group may also explain the faster performances. Conclusions: The role that ALDH2 plays in the pathology of cognitive impairment in opiate users may lead new focus in studies of the pathophysiology in opiate usage and its consequences on cognitive function.

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Mitochondrial aldehyde dehydrogenase polymorphism is not associated with incidence of Alzheimer's disease

Abstract: ALDH2*2 does not seem to be important in the etiology of dementia.

Cited by 23 publications

References 22 publications

The association of mitochondrial aldehyde dehydrogenase gene (ALDH2) polymorphism with susceptibility to late-onset Alzheimer's disease in Chinese

The association of mitochondrial aldehyde dehydrogenase gene (ALDH2) polymorphism with susceptibility to late-onset Alzheimer's disease in Chinese

Increased Mitochondrial Aldehydedehydrogenase in the putamen of individuals with Alzheimer's disease

Effect of Aldehyde Dehydrogenase 2 Gene Polymorphism on Executive Function in Opiate User

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