Erratum to “Alpha-lipoic acid as a new treatment option for Alzheimer type dementia” [Arch. Gerontol. Geriatr. 32 (2001) 275–282]

Häger, Klaus; Marahrens, Andres; Kenklies, Marlene; Riederer, Peter; Münch, Gerald

doi:10.1016/j.archger.2009.08.001

Cited by 11 publications

(7 citation statements)

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“…LA is used clinically to treat AD (Hager et al, 2007 , 2010 ; Fava et al, 2013 ), but the growing knowledge we provide on glucose metabolism restoration by LA via the BDNF/TrkB/HIF-1α pathway in AD may support a novel therapy target for neurodegenerative diseases (Nakamura et al, 2006 ; Li et al, 2012 ; Lin et al, 2014 ; Jiao et al, 2016 ). Our study supports LA as a critical supplement to reinstate brain glucose metabolism, which is involved in the upregulated expression of GLUT3, GLUT4, VEGF, OGG1/2, MTH1, and HK activity.…”

Section: Discussionmentioning

confidence: 99%

α-Lipoic Acid Maintains Brain Glucose Metabolism via BDNF/TrkB/HIF-1α Signaling Pathway in P301S Mice

Zhang

Yan

et al. 2020

Front. Aging Neurosci.

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The microtubule-associated protein tau is closely correlated with hypometabolism in Alzheimer's disease (AD). α-lipoic acid (LA), which is a naturally occurring cofactor in mitochondrial, has been shown to have properties that can inhibit the tau pathology and neuronal damage in our previous research. However, if LA affects glucose metabolism when it reverses tau pathology remains unclear, especially concerning the potential mechanism. Therefore, we make a further study using the P301S mouse model (a tauopathy and AD mouse model which overexpressing fibrillary tau) to gain a clear idea of the aforementioned problems. Here, we found chronic LA administration significantly increased glucose availability by elevating glucose transporter 3 (GLUT3), GLUT4, vascular endothelial growth factor (VEGF) protein and mRNA level, and heme oxygenase-1 (HO-1) protein level in P301S mouse brains. Meanwhile, we found that LA also promoted glycolysis by directly upregulating hexokinase (HK) activity, indirectly by increasing proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and DNA repair enzymes (OGG1/2 and MTH1). Further, we found the underlying mechanism of restored glucose metabolism might involve in the activation of brain-derived neurotrophic factor (BDNF)/tyrosine Kinase receptor B (TrkB)/hypoxia-inducible factor-1α (HIF-1α) signaling pathway by LA treatment.

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Section: Discussionmentioning

confidence: 99%

α-Lipoic Acid Maintains Brain Glucose Metabolism via BDNF/TrkB/HIF-1α Signaling Pathway in P301S Mice

Zhang

Yan

et al. 2020

Front. Aging Neurosci.

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“…Nine patients with AD and related dementias were given 600 mg LA for an average of 337 days. The treatment led to stabilization of cognitive functions as measured by the mini-mental state examination and the AD assessment scale, cognitive scale (ADAScog) [138]. In a follow-up study, the authors extended the analysis to 43 patients over an observation period of 48 months.…”

Section: Alzheimer's Diseasementioning

confidence: 99%

Lipoic Acid: A Novel Therapeutic Approach for Multiple Sclerosis and Other Chronic Inflammatory Diseases of the CNS

Salinthone

Yadav²,

Bourdette³

et al. 2008

EMIDDT

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The naturally occurring antioxidant lipoic acid (LA) was first described as an essential cofactor for the conversion of pyruvate to Acetyl-CoA, a critical step in respiration. LA is now recognized as a compound that has many biological functions. Along with its reduced form dihydrolipoic acid (DHLA), LA reduces and recycles cellular antioxidants such as glutathione, and chelates zinc, copper and other transition metal ions in addition to heavy metals. LA can also act as a scavenger of reactive oxygen and nitrogen species. By acting as an insulin mimetic agent, LA stimulates glucose uptake in many different cell types and can also modulate insulin signaling. The p38 and ERK MAP kinase pathways, AKT and NFkappaB are all regulated by LA. In addition, LA activates the prostaglandin EP2 and EP4 receptors to stimulate the production of the small molecule cyclic adenosine 5' monophosphate (cAMP). These diverse actions suggest that LA may be therapeutically effective in treating oxidative stress associated diseases. This review discusses the known biochemical properties of LA, its antioxidant properties, its ability to modulate signal transduction pathways, and the recent progress made in the utilization of LA as a therapeutic alternative for multiple sclerosis, Alzheimer's disease and diabetic neuropathy.

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“…A study conducted with 600 mg of alpha lipoic acid given daily to nine Alzheimer's patients, on an average for 80 days lead to stabilization of cognitive functions in the Alzheimer's study group. This was the first indication that alpha lipoic acid might be a successful neuroprotective therapy option for Alzheimer diseases and related dementias [21].…”

Section: Introductionmentioning

confidence: 99%

The effect of antioxidants in acute amitriptyline poisoning

Ali

Raja

2019

Toxicology Reports

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Objective To study the effect of Antioxidants supplementation in reducing oxidative stress induced in acute amitriptyline poisoning cases. Design and methods We compared the effect of supplementation of treatment of acute amitriptyline poisoning cases with alpha lipoic acid alone or with vitamin C, with that of those receiving only routine standard treatment (RST) as a control group. A total of 132 subjects divided into 5 groups were selected from IMCU (Intensive Medical Care Unit) and Toxicology Ward, Govt. General Hospital, Chennai, India. The study was restricted to grade 1 coma in poisoned subjects per the Edinburg scale. Each of the subjects was in the groups were supplemented with either placebo, RST, RST with vitamin C, RST with ALA, or RST with vitamin C and ALA. Acute anti-depressant poisoning (especially with amitriptyline) induced oxidative stress caused lipid peroxidation. Plasma cholinesterases (chE) play a major role in combating this effect. A determination of the level of cholinesterase (chE) acts as an indirect indicator of the level of oxidative stress and a measure of the efficacy of antioxidant supplementation. Plasma cholinesterase estimation was done by colorimetric method. The change in color of the indicator bromothymol blue caused by the liberated acetic acid from cholinesterase read by spectrophotometer at 620 nm was used to determine the levels of cholinesterase. Result A decrease in the level of oxidative stress was observed among those supplemented with either alpha lipoic acid alone or along with vitamin C, with a slightly more decrease in oxidative stress in the latter group. A p-value of <0.001 is considered significant statistically. The percentage of the benefit of treatment on supplementation with vitamin C and alpha lipoic acid showed a marked increase in group V (26.9%) cases after supplementation with both in combination. Conclusion The results provide evidence that the oxidative stress induced by acute amitriptyline poisoning is comparatively decreased by supplementation with antioxidants like alpha lipoic acid and vitamin C, than those only on routine standard treatment.

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Erratum to “Alpha-lipoic acid as a new treatment option for Alzheimer type dementia” [Arch. Gerontol. Geriatr. 32 (2001) 275–282]

Cited by 11 publications

References 0 publications

α-Lipoic Acid Maintains Brain Glucose Metabolism via BDNF/TrkB/HIF-1α Signaling Pathway in P301S Mice

α-Lipoic Acid Maintains Brain Glucose Metabolism via BDNF/TrkB/HIF-1α Signaling Pathway in P301S Mice

Lipoic Acid: A Novel Therapeutic Approach for Multiple Sclerosis and Other Chronic Inflammatory Diseases of the CNS

The effect of antioxidants in acute amitriptyline poisoning

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