The protective effect of metformin in scopolamine-induced learning and memory impairment in rats

Aksöz, Elif; Göçmez, S.S.; Şahin, Tuğçe Demirtaş; Akşit, Dilek; Akşit, Hasan; Utkan, Tijen

doi:10.1016/j.pharep.2019.04.015

Cited by 43 publications

(29 citation statements)

References 24 publications

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“…Furthermore, metformin was able to increase the hippocampal levels of antioxidant enzymes, such as superoxide dismutase levels [ 121 ]. These results give support to the hypothesis that metformin could be a potential preventive drug against cognitive and memory impairment [ 94 , 95 , 121 , 124 , 125 , 126 , 127 , 128 , 129 , 130 , 131 , 132 ] ( Table 1 ). Similarly, metformin was shown to prevent cognitive damage in the chronic L-methionine model of memory impairment, probably by normalizing oxidative damage [ 124 ].…”

Section: Molecular Mechanism Involved In Neuroprotective Effects Of Metformin In Alzheimer’s Diseasesupporting

confidence: 80%

“…Hence, it is accepted that insulin improves emotional function in active and elderly people, as well as Alzheimer’s patients [ 128 ]. Insulin signaling can influence the synaptic plasticity by controlling glutamate receptor expression and trafficking, and insulin receptors are enriched at hippocampal synapses, where they are proposed to control synaptic plasticity by interactions with the glutamatergic system [ 95 , 128 , 129 , 130 , 131 ]. Furthermore, various studies have shown that synaptic markers and/or dendritic spine dysfunction appear before the development of Aβ plaques and NFTs, thus implying that these events are closely linked to cognitive decline in AD [ 95 , 128 , 129 , 130 , 131 , 132 ].…”

Section: Molecular Mechanism Involved In Neuroprotective Effects Of Metformin In Alzheimer’s Diseasementioning

confidence: 99%

“…Insulin signaling can influence the synaptic plasticity by controlling glutamate receptor expression and trafficking, and insulin receptors are enriched at hippocampal synapses, where they are proposed to control synaptic plasticity by interactions with the glutamatergic system [ 95 , 128 , 129 , 130 , 131 ]. Furthermore, various studies have shown that synaptic markers and/or dendritic spine dysfunction appear before the development of Aβ plaques and NFTs, thus implying that these events are closely linked to cognitive decline in AD [ 95 , 128 , 129 , 130 , 131 , 132 ]. In older rhesus monkeys, selective loss of thin spines is closely associated with decreased learning capacity [ 134 , 135 , 136 ].…”

Section: Molecular Mechanism Involved In Neuroprotective Effects Of Metformin In Alzheimer’s Diseasementioning

confidence: 99%

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Metformin a Potential Pharmacological Strategy in Late Onset Alzheimer’s Disease Treatment

et al. 2021

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Alzheimer’s disease (AD) is one of the most devastating brain disorders. Currently, there are no effective treatments to stop the disease progression and it is becoming a major public health concern. Several risk factors are involved in the progression of AD, modifying neuronal circuits and brain cognition, and eventually leading to neuronal death. Among them, obesity and type 2 diabetes mellitus (T2DM) have attracted increasing attention, since brain insulin resistance can contribute to neurodegeneration. Consequently, AD has been referred to “type 3 diabetes” and antidiabetic medications such as intranasal insulin, glitazones, metformin or liraglutide are being tested as possible alternatives. Metformin, a first line antihyperglycemic medication, is a 5′-adenosine monophosphate (AMP)-activated protein kinase (AMPK) activator hypothesized to act as a geroprotective agent. However, studies on its association with age-related cognitive decline have shown controversial results with positive and negative findings. In spite of this, metformin shows positive benefits such as anti-inflammatory effects, accelerated neurogenesis, strengthened memory, and prolonged life expectancy. Moreover, it has been recently demonstrated that metformin enhances synaptophysin, sirtuin-1, AMPK, and brain-derived neuronal factor (BDNF) immunoreactivity, which are essential markers of plasticity. The present review discusses the numerous studies which have explored (1) the neuropathological hallmarks of AD, (2) association of type 2 diabetes with AD, and (3) the potential therapeutic effects of metformin on AD and preclinical models.

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Section: Molecular Mechanism Involved In Neuroprotective Effects Of Metformin In Alzheimer’s Diseasesupporting

confidence: 80%

Section: Molecular Mechanism Involved In Neuroprotective Effects Of Metformin In Alzheimer’s Diseasementioning

confidence: 99%

Section: Molecular Mechanism Involved In Neuroprotective Effects Of Metformin In Alzheimer’s Diseasementioning

confidence: 99%

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Metformin a Potential Pharmacological Strategy in Late Onset Alzheimer’s Disease Treatment

et al. 2021

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“…AD is the most common neurodegenerative disease and many pathological processes are involved in its emergence [58]. However, the hypothesis of amyloid cascade and the toxicity of amyloid beta (Aβ) peptides have dominated research so far due to advanced studies showing that aggregates of this peptide are characteristic signs of the disease [59,60,61].…”

Section: Bioactivities and Therapeutic Applications Of Bee Venom Amentioning

confidence: 99%

Bee Venom: Overview of Main Compounds and Bioactivities for Therapeutic Interests

et al. 2019

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Apitherapy is an alternate therapy that relies on the usage of honeybee products, most importantly bee venom for the treatment of many human diseases. The venom can be introduced into the human body by manual injection or by direct bee stings. Bee venom contains several active molecules such as peptides and enzymes that have advantageous potential in treating inflammation and central nervous system diseases, such as Parkinson’s disease, Alzheimer’s disease, and amyotrophic lateral sclerosis. Moreover, bee venom has shown promising benefits against different types of cancer as well as anti-viral activity, even against the challenging human immunodeficiency virus (HIV). Many studies described biological activities of bee venom components and launched preclinical trials to improve the potential use of apitoxin and its constituents as the next generation of drugs. The aim of this review is to summarize the main compounds of bee venom, their primary biological properties, mechanisms of action, and their therapeutic values in alternative therapy strategies.

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“…The length of interval between induction and MWM test with all methods varied with the different types of induction. The interval was 7 weeks on average, while the fastest was 30 min after induction (of scopolamine injection) [75], and the longest was 32 weeks (HFHG diet) [85]. The most widely used administration technique for introducing toxic substances was through the intracerebroventricular (ICV) route (Table 1).…”

Section: Toxic Substancesmentioning

confidence: 99%

Toxic Substance-induced Hippocampal Neurodegeneration in Rodents as Model of Alzheimer’s Dementia

Nurmasitoh

Sari

Susilowati

2021

Open Access Maced J Med Sci

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BACKGROUND: Alzheimer’s Dementia (AD) cases are increasing with the global elderly population. To study the part of the brain affected by AD, animal models for hippocampal degeneration are still necessary to better understand AD pathogenesis and develop treatment and prevention measures. AIM: This study was a systematic review of toxic substance-induced animal models of AD using the Morris Water Maze method in determining hippocampal-related memory impairment. Our aim was reviewing the methods of AD induction using toxic substances in laboratory rodents and evaluating the report of the AD biomarkers reported in the models. METHODS: Data were obtained from articles in the PubMed database, then compiled, categorized, and analyzed. Eighty studies published in the past 5 years were included for analysis. RESULTS AND DISCUSSION: The most widely used method was intracerebroventricular injection of amyloid-β _substances. However, some less technically challenging techniques using oral or intraperitoneal administration of other toxic substances also produce successful models. Instead of hippocampal neurodegeneration, many studies detected biomarkers of the AD pathological process while some reported inflammation, oxidative stress, neurotrophic factors, and changes of cholinergic activity. Female animals were underrepresented despite a high incidence of AD in women. CONCLUSION: Toxic substances may be used to develop AD animal models characterized with appropriate AD pathological markers. Characterization of methods with the most easy-handling techniques and more studies in female animal models should be encouraged.

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The protective effect of metformin in scopolamine-induced learning and memory impairment in rats

Cited by 43 publications

References 24 publications

Metformin a Potential Pharmacological Strategy in Late Onset Alzheimer’s Disease Treatment

Metformin a Potential Pharmacological Strategy in Late Onset Alzheimer’s Disease Treatment

Bee Venom: Overview of Main Compounds and Bioactivities for Therapeutic Interests

Toxic Substance-induced Hippocampal Neurodegeneration in Rodents as Model of Alzheimer’s Dementia

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