Alpha-lipoic acid-mediated activation of muscarinic receptors improves hippocampus- and amygdala-dependent memory

Mahboob, Aamra; Farhat, Syeda Mehpara; Iqbal, Ghazala; Babar, Mustafeez Mujtaba; Zaidi, Najam‐us‐Sahar Sadaf; Nabavi, Seyed Mohammad; Ahmed, Touqeer

doi:10.1016/j.brainresbull.2016.02.014

Cited by 30 publications

(12 citation statements)

References 52 publications

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“…Compelling evidence indicates that LA displays memory-ameliorating properties in a variety of experimental models of neurodegenerative diseases, as well as in memory decline associated with aging in rodents. Studies aiming to assess the neuroprotective effects of LA on behavioral outcomes showed that LA can reduce memory deficits in different behavioral paradigms on AD (Quinn et al, 2007 ; Farr et al, 2012 ), HD (Mehrotra et al, 2015 ), oxidative stress (Stoll et al, 1993 , 1994 ; Liu et al, 2002a ; Farr et al, 2003 ; Manda et al, 2007 ), and age-associated cognitive dysfunction (Cui et al, 2006 ; Mahboob et al, 2016 ) models. In humans, two studies in AD patients have supported the positive cognitive effects of LA (Hager et al, 2001 , 2007 ).…”

Section: Discussionmentioning

confidence: 99%

“…Cui et al ( 2006 ) evaluating a concomitant treatment with LA and d-Galactose exposure (used to induce memory loss and neurodegeneration) verified that LA ameliorated memory dysfunction in the Morris water maze task. Another study reported the neuroprotective effects of LA in neurotoxicity model induced by AlCl 3 administration to mice (Mahboob et al, 2016 ). LA enhanced fear memory and social novelty preference in comparison to the AlCl 3 -treated group.…”

Section: Effects Of La In Experimental Models Of Memory Deficits Assomentioning

confidence: 99%

“…In addition, the authors showed that the treatment with LA restored the parameters of total homocysteine (tHcy), insulin, insulin like growth factor-1 (IGF-1), interlukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Mahboob et al ( 2016 ), analyzed the effects of LA in AlCl 3 - model of neurodegeneration, demonstrating its capacity in ameliorating cognitive functions and enhancing cholinergic system functions. LA treatment increased the expression of muscarinic receptor genes M1, M2 and choline acetyltransferase (ChaT) relative to AlCl 3 -treated group.…”

Section: Putative Mechanisms Underlying La-induced Neuroprotective Efmentioning

confidence: 99%

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Potential Therapeutic Effects of Lipoic Acid on Memory Deficits Related to Aging and Neurodegeneration

Molz

Schröder

2017

Front. Pharmacol.

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The aging process comprises a series of organic alterations, affecting multiple systems, including the nervous system. Aging has been considered the main risk factor for the advance of neurodegenerative diseases, many of which are accompanied by cognitive impairment. Aged individuals show cognitive decline, which has been associated with oxidative stress, as well as mitochondrial, and consequently energetic failure. Lipoic acid (LA), a natural compound present in food and used as a dietary supplement, has been considered a promising agent for the treatment and/or prevention of neurodegenerative disorders. In spite of a number of preclinical studies showing beneficial effects of LA in memory functioning, and pointing to its neuroprotective potential effect, to date only a few studies have examined its effects in humans. Investigations performed in animal models of memory loss associated to aging and neurodegenerative disorders have shown that LA improves memory in a variety of behavioral paradigms. Moreover, cell and molecular mechanisms underlying LA effects have also been investigated. Accordingly, LA displays antioxidant, antiapoptotic, and anti-inflammatory properties in both in vivo and in vitro studies. In addition, it has been shown that LA reverses age-associated loss of neurotransmitters and their receptors, which can underlie its effects on cognitive functions. The present review article aimed at summarizing and discussing the main studies investigating the effects of LA on cognition as well as its cell and molecular effects, in order to improve the understanding of the therapeutic potential of LA on memory loss during aging and in patients suffering from neurodegenerative disorders, supporting the development of clinical trials with LA.

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Section: Discussionmentioning

confidence: 99%

Section: Effects Of La In Experimental Models Of Memory Deficits Assomentioning

confidence: 99%

Section: Putative Mechanisms Underlying La-induced Neuroprotective Efmentioning

confidence: 99%

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Potential Therapeutic Effects of Lipoic Acid on Memory Deficits Related to Aging and Neurodegeneration

Molz

Schröder

2017

Front. Pharmacol.

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“…After continuously injected for 3 days, the animals got 1 day off, and treatment was stopped when cumulative injection add up to 2 months. The dosage and treatment protocol of LA was determined according to previous studies (Maritim et al, 2003;Zhao et al, 2015;Mahboob et al, 2016). During chronic treatment with LA, the body weight and health conditions were monitored daily.…”

Section: Animals and Pharmacological Treatmentsmentioning

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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“…Besides, ALA has a potential role in cognitive and behavioural functions via the enhancement of the cholinergic process. Thus, it is an desirable curative agent for the cure of neurvous system disorders [17]. ALA has been demonstrated to have a mechanism of action interfered with pathogenic results of Alzhemier's disease which is also characterized by both a cholinergic deficit, and senile plaques (accumulation of betaamyloid).…”

Section: Potential Therapeutic Effects Of Alpha Lipoic Acid In Psychimentioning

confidence: 99%

Potential Therapeutic Agent In Psychiatric And Neurological Diseases: Alpha Lipoic Acid

Çekici¹,

BakÃ„Â±rhan²

2018

Acta Psychopathol

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Alpha-lipoic acid-mediated activation of muscarinic receptors improves hippocampus- and amygdala-dependent memory

Cited by 30 publications

References 52 publications

Potential Therapeutic Effects of Lipoic Acid on Memory Deficits Related to Aging and Neurodegeneration

Potential Therapeutic Effects of Lipoic Acid on Memory Deficits Related to Aging and Neurodegeneration

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

Potential Therapeutic Agent In Psychiatric And Neurological Diseases: Alpha Lipoic Acid

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