Nootropic effect of neferine on aluminium chloride–induced Alzheimer's disease in experimental models

2019 ◽  
Vol 34 (2) ◽  
Author(s):  
Shuaizeng Yin ◽  
Qin Ran ◽  
Jin Yang ◽  
Yuhua Zhao ◽  
Chenyu Li
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Experimental Models ◽  
Aluminium Chloride ◽  
Nootropic Effect

Effect of artesunate in an animal model of Aluminium chloride induced alzheimer's disease

2021 ◽  
Vol 14 (2) ◽  
pp. 633-639
Author(s):  
Praveen S E Kumar ◽  
K L Bairy ◽  
Veena Nayak ◽  
Mohandas Rao ◽  
Shiva Kumar Reddy ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Model ◽  
Aluminium Chloride

scholarly journals Red Ginseng Attenuates Aβ-Induced Mitochondrial Dysfunction and Aβ-mediated Pathology in an Animal Model of Alzheimer’s Disease

2019 ◽  
Vol 20 (12) ◽  
pp. 3030 ◽  
Author(s):  
Soo Jung Shin ◽  
Seong Gak Jeon ◽  
Jin-il Kim ◽  
Yu-on Jeong ◽  
Sujin Kim ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Hippocampal Formation ◽  
Experimental Models ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Red Ginseng ◽  
Model Of Alzheimer’S Disease

Alzheimer’s disease (AD) is the most common neurodegenerative disease and is characterized by neurodegeneration and cognitive deficits. Amyloid beta (Aβ) peptide is known to be a major cause of AD pathogenesis. However, recent studies have clarified that mitochondrial deficiency is also a mediator or trigger for AD development. Interestingly, red ginseng (RG) has been demonstrated to have beneficial effects on AD pathology. However, there is no evidence showing whether RG extract (RGE) can inhibit the mitochondrial deficit-mediated pathology in the experimental models of AD. The effects of RGE on Aβ-mediated mitochondrial deficiency were investigated in both HT22 mouse hippocampal neuronal cells and the brains of 5XFAD Aβ-overexpressing transgenic mice. To examine whether RGE can affect mitochondria-related pathology, we used immunohistostaining to study the effects of RGE on Aβ accumulation, neuroinflammation, neurodegeneration, and impaired adult hippocampal neurogenesis in hippocampal formation of 5XFAD mice. In vitro and in vivo findings indicated that RGE significantly improves Aβ-induced mitochondrial pathology. In addition, RGE significantly ameliorated AD-related pathology, such as Aβ deposition, gliosis, and neuronal loss, and deficits in adult hippocampal neurogenesis in brains with AD. Our results suggest that RGE may be a mitochondria-targeting agent for the treatment of AD.

scholarly journals Microglial Progranulin: Involvement in Alzheimer’s Disease and Neurodegenerative Diseases

Cells ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 230 ◽  
Author(s):  
Anarmaa Mendsaikhan ◽  
Ikuo Tooyama ◽  
Douglas G. Walker
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurodegenerative Diseases ◽  
Neuronal Ceroid Lipofuscinosis ◽  
Experimental Models ◽  
Lysosomal Storage ◽  
Cellular Functions ◽  
New Treatments ◽  
Regulatory Properties ◽  
Microglial Inflammation

Neurodegenerative diseases such as Alzheimer’s disease have proven resistant to new treatments. The complexity of neurodegenerative disease mechanisms can be highlighted by accumulating evidence for a role for a growth factor, progranulin (PGRN). PGRN is a glycoprotein encoded by the GRN/Grn gene with multiple cellular functions, including neurotrophic, anti-inflammatory and lysosome regulatory properties. Mutations in the GRN gene can lead to frontotemporal lobar degeneration (FTLD), a cause of dementia, and neuronal ceroid lipofuscinosis (NCL), a lysosomal storage disease. Both diseases are associated with loss of PGRN function resulting, amongst other features, in enhanced microglial neuroinflammation and lysosomal dysfunction. PGRN has also been implicated in Alzheimer’s disease (AD). Unlike FTLD, increased expression of PGRN occurs in brains of human AD cases and AD model mice, particularly in activated microglia. How microglial PGRN might be involved in AD and other neurodegenerative diseases will be discussed. A unifying feature of PGRN in diseases might be its modulation of lysosomal function in neurons and microglia. Many experimental models have focused on consequences of PGRN gene deletion: however, possible outcomes of increasing PGRN on microglial inflammation and neurodegeneration will be discussed. We will also suggest directions for future studies on PGRN and microglia in relation to neurodegenerative diseases.

scholarly journals Melatonin and Its Agonist Ramelteon in Alzheimer's Disease: Possible Therapeutic Value

2011 ◽  
Vol 2011 ◽  
pp. 1-15 ◽  
Author(s):  
Venkatramanujam Srinivasan ◽  
Charanjit Kaur ◽  
Seithikurippu Pandi-Perumal ◽  
Gregory M. Brown ◽  
Daniel P. Cardinali
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Sleep Disturbances ◽  
Amyloid Β ◽  
Signs And Symptoms ◽  
Experimental Models ◽  
Melatonin Receptors ◽  
Postmortem Brain ◽  
Amyloid Β Protein ◽  
Therapeutic Value

Alzheimer's disease (AD) is an age-associated neurodegenerative disease characterized by the progressive loss of cognitive function, loss of memory and insomnia, and abnormal behavioral signs and symptoms. Among the various theories that have been put forth to explain the pathophysiology of AD, the oxidative stress induced by amyloid β-protein (Aβ) deposition has received great attention. Studies undertaken on postmortem brain samples of AD patients have consistently shown extensive lipid, protein, and DNA oxidation. Presence of abnormal tau protein, mitochondrial dysfunction, and protein hyperphosphorylation all have been demonstrated in neural tissues of AD patients. Moreover, AD patients exhibit severe sleep/wake disturbances and insomnia and these are associated with more rapid cognitive decline and memory impairment. On this basis, the successful management of AD patients requires an ideal drug that besides antagonizing Aβ-induced neurotoxicity could also correct the disturbed sleep-wake rhythm and improve sleep quality. Melatonin is an effective chronobiotic agent and has significant neuroprotective properties preventing Aβ-induced neurotoxic effects in a number of animal experimental models. Since melatonin levels in AD patients are greatly reduced, melatonin replacement has the potential value to be used as a therapeutic agent for treating AD, particularly at the early phases of the disease and especially in those in whom the relevant melatonin receptors are intact. As sleep deprivation has been shown to produce oxidative damage, impaired mitochondrial function, neurodegenerative inflammation, and altered proteosomal processing with abnormal activation of enzymes, treatment of sleep disturbances may be a priority for arresting the progression of AD. In this context the newly introduced melatonin agonist ramelteon can be of much therapeutic value because of its highly selective action on melatonin MT1/MT2receptors in promoting sleep.

scholarly journals Antiepileptic drugs as a new therapeutic concept for the prevention of cognitive impairment and Alzheimer’s disease. Recent advances

2015 ◽  
Vol 23 (2) ◽  
pp. 139-147 ◽  
Author(s):  
Krzysztof Sendrowski ◽  
Wojciech Sobaniec
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Antiepileptic Drugs ◽  
Clinical Studies ◽  
Experimental Models ◽  
Brain Pathology ◽  
Therapeutic Concept ◽  
Neuronal Hyperexcitability ◽  
Pubmed Database

SummaryIntroduction.Excessive accumulation of amyloid-beta (Aβ) peptides in the brain results initially in mild cognitive impairment (MCI) and finally in Alzheimer’s disease (AD). Evidences from experimental and clinical studies show that pathological hyperexcitability of hippocampal neurons is a very early functional impairment observed in progressive memory dysfunctions. Therefore, antiepileptic drugs (AEDs) whose mechanism of action is aimed at inhibition of such neuronal hyperexcitability, seems to be an rationale choice for MCI and AD treatment.Aim.To provide data from experimental and clinical studies on: 1. The unfavorable impact of neuronal hyperexcitability, mainly within the hippocampus, on cognitive processes. 2. Efficacy of AEDs against such abnormally elevated neuronal activity for the prevention of progressive cognitive impairment.Methods.A literature review of publications published within the last fifteen years, was conducted using the PubMed database.Review.The authors describe Aβ-induced hyperexcitability of hippocampal nerve cells as the cause of cognitive deficits, the connection of such activity with an increased risk of seizures and epilepsy in patients with MCI/AD, and finally the efficacy of AEDs: valproic acid (VPA), phenytoin (PHT), topiramate (TPM), lamotrigine (LTG), ethosuximide (ESM) and levetiracetam (LEV) in the prevention of cognitive impairment in experimental models and patients with MCI/AD.Conclusions.The majority of the studied AEDs improve cognitive dysfunction in various experimental models of Aβ-induced brain pathology with accompanied neuronal hyperexcitability. The promising results achieved for LEV in animal models of cognitive impairment were also confirmed in patients with MCI/AD. LEV was well-tolerated and it’s beneficial antidementive effect was confirmed by memory tests and fMRI examination. In conclusion, the use of AEDs could be a novel therapeutic concept for preventing cognitive impairment in patients with Aβ-associated brain pathology.

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