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Article ; Online: Protective effects of Embelin in Benzo[α]pyrene induced cognitive and memory impairment in experimental model of mice.

Goal, Akansh / Raj, Khadga / Singh, Shamsher / Arora, Rimpi

Current research in neurobiology

2024 Volume 6, Page(s) 100122

Abstract: Alzheimer's disease (AD) is a neurodegenerative disease that affects the neurons in the hippocampus, resulting in cognitive and memory impairment. The most prominent clinical characteristics of AD are the production of amyloid-beta (Aβ) plaques, ... ...

Abstract	Alzheimer's disease (AD) is a neurodegenerative disease that affects the neurons in the hippocampus, resulting in cognitive and memory impairment. The most prominent clinical characteristics of AD are the production of amyloid-beta (Aβ) plaques, neurofibrillary tangles, and neuroinflammation in neurons. It has been proven that embelin (Emb) possesses antioxidant, anti-inflammatory, and neuroprotective properties. Therefore, we assessed the therapeutic potential of Emb in Benzo [α]pyrene (BaP)-induced cognitive impairment in experimental mice. BaP (5 mg/kg, i. p) was given to mice daily for 28 days, and Emb (2.5, 5, and 10 mg/kg, i. p) was given from 14 to 28 days of a protocol. In addition, locomotor activity was evaluated using open-field and spatial working, and non-spatial memory was evaluated using novel object recognition tasks (NORT), Morris water maze (MWM), and Y- maze. At the end of the study, the animal tissue homogenate was used to check biochemicals, neuroinflammation, and neurotransmitter changes. BaP-treated mice showed a significant decline in locomotor activity, learning and memory deficits and augmented oxidative stress (lipid peroxidation, nitrite, and GSH). Further, BaP promoted the release of inflammatory tissue markers, decreased acetylcholine, dopamine, GABA, serotonin, and norepinephrine, and increased glutamate concentration. However, treatment with Emb at dose-dependently prevented biochemical changes, improved antioxidant levels, reduced neuroinflammation, restored neurotransmitter concentration, and inhibited the NF-κB pathway. The current study's finding suggested that Emb improved cognitive functions through antioxidant, anti-inflammatory, and neuroprotective mechanisms and inhibition of acetylcholinesterase (AChE) enzyme activities and Aβ-42 accumulation.
Language	English
Publishing date	2024-01-05
Publishing country	Netherlands
Document type	Journal Article
ISSN	2665-945X
ISSN (online)	2665-945X
DOI	10.1016/j.crneur.2023.100122
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Article ; Online: L-theanine attenuates LPS-induced motor deficit in experimental rat model of Parkinson's disease: emphasis on mitochondrial activity, neuroinflammation, and neurotransmitters.

Kumar, Shivam / Awasthi, Anupam / Raj, Khadga / Singh, Shamsher

Psychopharmacology

2023 Volume 240, Issue 7, Page(s) 1493–1508

Abstract: Rationale: Parkinson's disease (PD) is a neurodegenerative disorder characterized by loss of dopaminergic neurons. The pathogenesis of PD includes oxidative stress, mitochondrial dysfunction, neuroinflammation, and neurotransmitter dysregulation. L- ... ...

Abstract	Rationale: Parkinson's disease (PD) is a neurodegenerative disorder characterized by loss of dopaminergic neurons. The pathogenesis of PD includes oxidative stress, mitochondrial dysfunction, neuroinflammation, and neurotransmitter dysregulation. L-theanine is found in green tea and has antioxidant, anti-inflammatory, and neuroprotective effects with a high blood brain barrier permeability. Objective: The objective of this study was to investigate the possible neuroprotective effect of L-theanine in lipopolysaccharide (LPS) induced motor deficits and striatal neurotoxicity in a rat model of PD. Methods: LPS was infused at a dose of 5 μg/5 μl PBS stereotaxically into SNpc of rats. Treatment with L-theanine (50 and 100 mg/kg; po) and Sinemet (36 mg/kg; po) was given from day 7 to 21 in of LPS injected rat. On a weekly basis all behavioral parameters were assessed, and animals were sacrificed on day 22. The striatum tissue of brain was isolated for biochemicals (Nitrite, GSH, catalase, SOD, mitochondrial complexes I and IV), neuroinflammatory markers, and neurotransmitters (serotonin, dopamine, norepinephrine, GABA, and glutamate) estimations. Results: Results revealed that L-theanine dose-dependently and significantly reversed motor deficits, assessed through locomotor and rotarod activity. Moreover, L-theanine attenuated biochemical markers, reduced oxidative stress, and neurotransmitters dysbalance in the brain. L-theanine treatment at 100 mg/kg; po substantially reduced these pathogenic events by increasing mitochondrial activity, restoring neurotransmitter levels, and inhibiting neuroinflammation. Conclusions: These data suggest that the positive effects of L-theanine on motor coordination may be mediated by the suppression of NF-κB induced by LPS. Therefore, L-theanine would have a new therapeutic potential for PD.
MeSH term(s)	Rats ; Animals ; Parkinson Disease/drug therapy ; Lipopolysaccharides/toxicity ; Neuroinflammatory Diseases ; Neurotransmitter Agents/pharmacology ; Glutamic Acid ; Neuroprotective Agents/pharmacology ; Neuroprotective Agents/therapeutic use ; Mitochondria ; Disease Models, Animal
Chemical Substances	theanine (8021PR16QO) ; Lipopolysaccharides ; Neurotransmitter Agents ; Glutamic Acid (3KX376GY7L) ; Neuroprotective Agents
Language	English
Publishing date	2023-05-16
Publishing country	Germany
Document type	Journal Article
ZDB-ID	130601-7
ISSN	1432-2072 ; 0033-3158
ISSN (online)	1432-2072
ISSN	0033-3158
DOI	10.1007/s00213-023-06382-y
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Article ; Online: Cladribine induces apoptosis, neuroinflammation, mitochondrial oxidative stress, tau phosphorylation and Aβ (1-42) pathway in the hippocampus: An in vivo approach.

Aran, Khadga Raj / Gupta, G D / Singh, Shamsher

Journal of chemical neuroanatomy

2023 Volume 133, Page(s) 102340

Abstract: Cladribine is a purine nucleoside found to enhance toxic amyloid protein and cause memory impairment. Patients following chemotherapy treatment commonly suffer from cognitive deficits more prevalent in the elderly than adults. A previous research study ... ...

Abstract	Cladribine is a purine nucleoside found to enhance toxic amyloid protein and cause memory impairment. Patients following chemotherapy treatment commonly suffer from cognitive deficits more prevalent in the elderly than adults. A previous research study revealed that cladribine has a high affinity to the brain, increases the level of amyloid precursor protein, and results in learning deficits. The study was designed to validate an animal model of cladribine administration to rats through mitochondrial oxidative stress, inflammation, apoptosis, tau phosphorylation, and amyloid-β (1-42) accumulation. In this study, all rats were orally given cladribine (0.5 and 1 mg/kg) for 28 days, resulting in impaired spatial memory confirmed by behavioural activity. On day 29, all rats were euthanized, and the hippocampal tissues were isolated and used for the estimation of neuroinflammatory markers, biochemicals parameters (glutathione, catalase, lipid peroxidation, and nitrite), amyloid-β (1-42) level, neurotransmitters, and nuclear factor kappa B analysis. Cladribine administration significantly elevated cytokines release, dysbalanced neurotransmitter concentration, and promoted the Aβ accumulation and hyperphosphorylation of tau protein. Our study outcome confirmed that cladribine produces cognitive impairment via activation of Nuclear factor kappa B, mitochondrial oxidative stress and dysbalanced of the endogenous antioxidant defence system.
MeSH term(s)	Humans ; Rats ; Animals ; Aged ; tau Proteins/metabolism ; Alzheimer Disease/metabolism ; Cladribine/pharmacology ; Cladribine/metabolism ; Cladribine/therapeutic use ; Phosphorylation ; NF-kappa B/metabolism ; Neuroinflammatory Diseases ; Hippocampus/metabolism ; Amyloid beta-Peptides/metabolism ; Apoptosis ; Oxidative Stress ; Disease Models, Animal
Chemical Substances	tau Proteins ; Cladribine (47M74X9YT5) ; NF-kappa B ; Amyloid beta-Peptides
Language	English
Publishing date	2023-09-13
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639443-7
ISSN	1873-6300 ; 0891-0618
ISSN (online)	1873-6300
ISSN	0891-0618
DOI	10.1016/j.jchemneu.2023.102340
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Article ; Online: Microbiota- Brain-Gut-Axis Relevance to Parkinson's Disease: Potential Therapeutic Effects of Probiotics.

Raj, Khadga / Singh, Shamsher / Chib, Shivani / Mallan, Sudhanshu

Current pharmaceutical design

2022 Volume 28, Issue 37, Page(s) 3049–3067

Abstract: Parkinson's disease (PD) is the second most common type of neurogenerative disease among middleaged and older people, characterized by aggregation of alpha-synuclein and dopaminergic neuron loss. The microbiota- gut-brain axis is a dynamic bidirectional ... ...

Abstract	Parkinson's disease (PD) is the second most common type of neurogenerative disease among middleaged and older people, characterized by aggregation of alpha-synuclein and dopaminergic neuron loss. The microbiota- gut-brain axis is a dynamic bidirectional communication network and is involved in the pathogenesis of PD. The aggregation of misfolded protein alpha-synuclein is a neuropathological characteristic of PD, originates in the gut and migrates to the central nervous system (CNS) through the vagus nerve and olfactory bulb. The change in the architecture of gut microbiota increases the level short-chain fatty acids (SCFAs) and other metabolites, acting on the neuroendocrine system and modulating the concentrations of gamma-Aminobutyric acid (GABA), serotonin, and other neurotransmitters. It also alters the vagus and intestinal signalling, influencing the brain and behaviour by activating microglia and systemic cytokines. Both experimental and clinical reports indicate the role of intestinal dysbiosis and microbiota host interaction in neurodegeneration. Probiotics are live microorganisms that modify the gut microbiota in the small intestine to avoid neurological diseases. Probiotics have been shown in clinical and preclinical studies to be effective in the treatment of PD by balancing the gut microbiota. In this article, we described the role of gut-microbiota in the pathogenesis of PD. The article aims to explore the mechanistic strategy of the gut-brain axis and its relation with motor impairment and the use of probiotics to maintain gut microbial flora and prevent PD-like symptoms.
MeSH term(s)	Aged ; Humans ; alpha-Synuclein/metabolism ; Brain/metabolism ; Gastrointestinal Microbiome/physiology ; Parkinson Disease/drug therapy ; Parkinson Disease/metabolism ; Probiotics/therapeutic use ; Brain-Gut Axis
Chemical Substances	alpha-Synuclein
Language	English
Publishing date	2022-10-06
Publishing country	United Arab Emirates
Document type	Journal Article ; Review
ZDB-ID	1304236-1
ISSN	1873-4286 ; 1381-6128
ISSN (online)	1873-4286
ISSN	1381-6128
DOI	10.2174/1381612828666221003112300
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Article ; Online: Protective effects of cerebrolysin against chemotherapy (carmustine) induced cognitive impairment in Albino mice.

Sharma, Suraj / Raj, Khadga / Singh, Shamsher

Drug and chemical toxicology

2021 Volume 45, Issue 6, Page(s) 2769–2779

Abstract: Chemotherapy-induced cognitive impairment (CICI) comprises different neurological problems, including difficulty in learning new things, concentrating and making decisions that affect daily life activities. Clinical reports indicate that around 70% of ... ...

Abstract	Chemotherapy-induced cognitive impairment (CICI) comprises different neurological problems, including difficulty in learning new things, concentrating and making decisions that affect daily life activities. Clinical reports indicate that around 70% of cancer patients receiving chemotherapy suffer from cognitive impairment. The purpose of the present study is to examine the effects of widely used anticancer medication (Carmustine) on cognitive function using mice model and investigation of the neuroprotective effects of Cerebrolysin (CBN). Cerebrolysin (CBN) is a mixture of several neurotrophic factors and active peptides with anti-inflammatory, antioxidant, and neuroprotective actions. Our study aimed to establish a mice model of Carmustine (BCNU)-induced cognitive deficits and determine the protective effects of CBN. BCNU (10 mg/kg, i.v.) was administered to mice for 28 days, and behavioral parameters were measured on a weekly basis. CBN (44 and 88 mg/kg, i.p.) was administered daily from day 1 to 28 to BCNU treatment mice. All animals were sacrificed on day 29 and brain hippocampus tissues were used for biochemical, neuroinflammatory, neurotransmitters analysis. BCNU administration animals showed impaired cognition and memory, confirmed from behavioral analysis. Further, BCNU increased oxidative stress, inflammatory cytokines release and altered neurotransmitters concentration as compared to the control group (
MeSH term(s)	Animals ; Mice ; Antioxidants/pharmacology ; Antioxidants/therapeutic use ; Carmustine/adverse effects ; Carmustine/therapeutic use ; Carmustine/toxicity ; Cognitive Dysfunction/chemically induced ; Cognitive Dysfunction/drug therapy ; Cognitive Dysfunction/prevention & control ; Cytokines ; Disease Models, Animal ; Nerve Growth Factors/therapeutic use ; Neuroprotective Agents/pharmacology ; Neurotransmitter Agents
Chemical Substances	Antioxidants ; Carmustine (U68WG3173Y) ; cerebrolysin (37KZM6S21G) ; Cytokines ; Nerve Growth Factors ; Neuroprotective Agents ; Neurotransmitter Agents
Language	English
Publishing date	2021-10-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	548368-2
ISSN	1525-6014 ; 0148-0545
ISSN (online)	1525-6014
ISSN	0148-0545
DOI	10.1080/01480545.2021.1991195
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Article ; Online: Spermine protects aluminium chloride and iron-induced neurotoxicity in rat model of Alzheimer's disease via attenuation of tau phosphorylation, Amyloid-β (1-42) and NF-κB pathway.

Raj, Khadga / Gupta, G D / Singh, Shamsher

Inflammopharmacology

2021 Volume 29, Issue 6, Page(s) 1777–1793

Abstract: Alzheimer's disease (AD) is the most prevalent type of dementia, characterized by a gradual decline in cognitive and memory functions of the aged peoples. Long-term exposure to heavy metals (aluminium and iron) cause neurotoxicity by amyloid plaques ... ...

Abstract	Alzheimer's disease (AD) is the most prevalent type of dementia, characterized by a gradual decline in cognitive and memory functions of the aged peoples. Long-term exposure to heavy metals (aluminium and iron) cause neurotoxicity by amyloid plaques accumulation, tau phosphorylation, increased oxidative stress, neuroinflammation, and cholinergic neurons degeneration, contributes to the development of AD-like symptoms. The present research work is designed to investigate the neuroprotective effect of spermine in aluminium chloride (AlCl
MeSH term(s)	Aluminum Chloride ; Alzheimer Disease/drug therapy ; Alzheimer Disease/physiopathology ; Amyloid beta-Peptides/metabolism ; Animals ; Antioxidants/administration & dosage ; Antioxidants/pharmacology ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Iron ; Male ; Maze Learning/drug effects ; NF-kappa B/metabolism ; Neuroinflammatory Diseases/drug therapy ; Neuroinflammatory Diseases/physiopathology ; Neuroprotective Agents/administration & dosage ; Neuroprotective Agents/pharmacology ; Oxidative Stress/drug effects ; Peptide Fragments/metabolism ; Phosphorylation ; Rats ; Rats, Wistar ; Spermine/administration & dosage ; Spermine/pharmacology ; tau Proteins/metabolism
Chemical Substances	Amyloid beta-Peptides ; Antioxidants ; NF-kappa B ; Neuroprotective Agents ; Peptide Fragments ; amyloid beta-protein (1-42) ; tau Proteins ; Spermine (2FZ7Y3VOQX) ; Aluminum Chloride (3CYT62D3GA) ; Iron (E1UOL152H7)
Language	English
Publishing date	2021-11-02
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1080058-x
ISSN	1568-5608 ; 0925-4692
ISSN (online)	1568-5608
ISSN	0925-4692
DOI	10.1007/s10787-021-00883-y
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Article ; Online: l-Theanine ameliorates motor deficit, mitochondrial dysfunction, and neurodegeneration against chronic tramadol induced rats model of Parkinson's disease.

Raj, Khadga / Gupta, G D / Singh, Shamsher

Drug and chemical toxicology

2021 Volume 45, Issue 5, Page(s) 2097–2108

Abstract: Parkinson's disease (PD) is the second most prevalent progressive neurodegenerative disease, characterized by loss of dopaminergic neurons in substantia nigra, with deficiency of dopamine in the striatum. Tramadol is safe analgesic but long-term use ... ...

Abstract	Parkinson's disease (PD) is the second most prevalent progressive neurodegenerative disease, characterized by loss of dopaminergic neurons in substantia nigra, with deficiency of dopamine in the striatum. Tramadol is safe analgesic but long-term use confirmed to elevate oxidative stress, neuroinflammation, mitochondrial dysfunction, in brain leads to motor deficits. l-Theanine is an active constituent of green tea which prevents neuronal loss, mitochondrial failure and improves dopamine, gamma-aminobutyric acid (GABA), serotonin levels and in the central nervous system (CNS) via antioxidant, anti-inflammatory, and neuromodulatory properties. In the present study, tramadol was injected intraperitoneally to Wister rats for 28 days at a dose of 50 mg/kg. l-Theanine (25, 50, and 100 mg/kg) was administered orally 3 h before tramadol administration from day 14 to day 28. Behavioral analyses including rotarod, narrow beam walk, open field, and grip strength were used to evaluate motor coordination on a weekly basis. On the day 29, all Wistar rats were sacrificed and striatum homogenates were used for biochemical (lipid peroxidation, nitrite, glutathione, glutathione peroxidase activity, superoxide dismutase, catalase, mitochondrial complex I, IV, and cyclic adenosine monophosphate), neuroinflammatory markers (tumor necrosis factor-α, interleukin-1β, and interleukin-17), and neurotransmitters (dopamine, norepinephrine, serotonin, GABA, and glutamate) analysis. Chronic tramadol treatment caused motor deficits reduced antioxidant enzymes level, increased striatal proinflammatory cytokines release, dysbalanced neurotransmitters, and reduced mitochondrial complex activity I, IV, and cAMP activity. However, l-theanine administration attenuated behavioral, biochemical, neuroinflammatory, neurotransmitters, and mitochondrial activity indicated it as a promising neuroprotective potential against degenerative changes in experimental model of PD.
MeSH term(s)	Animals ; Antioxidants/metabolism ; Antioxidants/pharmacology ; Corpus Striatum/metabolism ; Disease Models, Animal ; Dopamine/metabolism ; Dopamine/pharmacology ; Glutamates/metabolism ; Glutamates/pharmacology ; Mitochondria ; Neurodegenerative Diseases/drug therapy ; Neurodegenerative Diseases/metabolism ; Neuroprotective Agents/pharmacology ; Neurotransmitter Agents/metabolism ; Oxidative Stress ; Parkinson Disease/drug therapy ; Parkinson Disease/metabolism ; Rats ; Rats, Wistar ; Serotonin ; Tramadol/metabolism ; Tramadol/pharmacology ; gamma-Aminobutyric Acid/metabolism ; gamma-Aminobutyric Acid/pharmacology
Chemical Substances	Antioxidants ; Glutamates ; Neuroprotective Agents ; Neurotransmitter Agents ; Serotonin (333DO1RDJY) ; Tramadol (39J1LGJ30J) ; gamma-Aminobutyric Acid (56-12-2) ; theanine (8021PR16QO) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2021-07-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	548368-2
ISSN	1525-6014 ; 0148-0545
ISSN (online)	1525-6014
ISSN	0148-0545
DOI	10.1080/01480545.2021.1907909
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Article ; Online: Neuroprotective Effect of Fucoxanthin against Intracerebroventricular Streptozotocin (ICV-STZ) Induced Cognitive Impairment in Experimental Rats.

Dhami, Mahadev / Raj, Khadga / Singh, Shamsher

Current Alzheimer research

2021 Volume 18, Issue 8, Page(s) 623–637

Abstract: Background: Alzheimer's disease (AD) is a neurological disorder characterized by loss of memory and cognitive functions caused by oxidative stress, neuroinflammation, change in neurotransmitter levels, and excessive deposition of Aβ: Objective: In ... ...

Abstract	Background: Alzheimer's disease (AD) is a neurological disorder characterized by loss of memory and cognitive functions caused by oxidative stress, neuroinflammation, change in neurotransmitter levels, and excessive deposition of Aβ Objective: In the present study, fucoxanthin was employed as a protective strategy in Intracerebroventricular Streptozotocin (ICV-STZ) induced experimental model of cognitive impairment. Methods: STZ was injected twice ICV (3 mg/kg) on alternate days 1 and 3, and Wistar rats were evaluated for the memory analysis using Morris water maze and elevated plus-maze. Fucoxanthin at low 50 mg/kg, p.o. and high dose 100 mg/kg, p.o. was administered for 14 days. All animals were sacrificed on day 29, and brain hippocampus tissue after isolation was used for biochemical (MDA, nitrite, GSH, SOD and Catalase), neuroinflammatory (TNF-α, IL-1β, and IL-6), neurotransmitters (ACh, GABA Glutamate), Aβ Results: STZ-infused rats showed significant impairment in learning and memory, increased oxidative stress (MDA, nitrite), reduced antioxidant defense (GSH, SOD and Catalase), promoted cytokine release, and change in neurotransmitters level. However, fucoxanthin improved cognitive functions, restored antioxidant levels, reduced inflammatory markers dose-dependently, and restored neurotransmitters concentration. Conclusion: The finding of the current study suggests that fucoxanthin could be the promising compound for improving cognitive functions through antioxidant, anti-inflammatory, and neuroprotective mechanisms, and inhibition of acetylcholinesterase (AChE) enzyme activities, Aβ
MeSH term(s)	Acetylcholinesterase/metabolism ; Animals ; Cognitive Dysfunction/chemically induced ; Cognitive Dysfunction/drug therapy ; Disease Models, Animal ; Maze Learning ; Neuroprotective Agents/therapeutic use ; Oxidative Stress ; Rats ; Rats, Wistar ; Streptozocin/toxicity ; Xanthophylls
Chemical Substances	Neuroprotective Agents ; Xanthophylls ; fucoxanthin (06O0TC0VSM) ; Streptozocin (5W494URQ81) ; Acetylcholinesterase (EC 3.1.1.7)
Language	English
Publishing date	2021-11-18
Publishing country	United Arab Emirates
Document type	Journal Article
ZDB-ID	2205170-3
ISSN	1875-5828 ; 1567-2050
ISSN (online)	1875-5828
ISSN	1567-2050
DOI	10.2174/1567205018666211118144602
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Article: Coronavirus as silent killer: recent advancement to pathogenesis, therapeutic strategy and future perspectives.

Raj, Khadga / Rohit / Ghosh, Anirban / Singh, Shamsher

Virusdisease

2020 Volume 31, Issue 2, Page(s) 137–145

Abstract: The present outbreak associated with corona virus [CoVs] in China which is believed to be one of the massive eruptions towards mankind in 2019-2020. In the present scenario CoVs has been transmitted to the European and American regions through the ... ...

Abstract	The present outbreak associated with corona virus [CoVs] in China which is believed to be one of the massive eruptions towards mankind in 2019-2020. In the present scenario CoVs has been transmitted to the European and American regions through the travellers from wide spread countries like China and Japan. The viral disease is spreading through the contact in any form by the infected persons or patients and creating huge risk of mortality. CoVs are a single positive-sense RNA virus; mutation rates are higher than DNA viruses and indicate a more effective survival adaption mechanism. Human CoVs can cause common cold and influenza-like illness and a variety of severe acute respiratory disease such as pneumonia. Early in infection, CoVs infects epithelial cells, macrophages, T-cells, dendritic cells and also can affect the development and implantation of pro-inflammatory cytokines and chemokines. It mainly produces the melanoma differentiation associated with protein-5, retinoic acid inducible gene-1 and endosomal toll-like receptor 3. How CoVs affects the function of the immune system is still unclear due to lack of this knowledge. No Food and Drug Administration approved treatment is available till date. In this review, we are tried to explore the epidemiology, pathogenesis and current treatment of CoVs infection. The promising therapeutics molecules against CoVs and future prospective have been also discussed which will be helpful for researchers to find out the new molecules for the treatment of CoVs disease.
Keywords	covid19
Language	English
Publishing date	2020-04-20
Publishing country	India
Document type	Journal Article ; Review
ZDB-ID	2846993-8
ISSN	2347-3517 ; 2347-3584
ISSN (online)	2347-3517
ISSN	2347-3584
DOI	10.1007/s13337-020-00580-4
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Article ; Online: Allicin ameliorates aluminium- and copper-induced cognitive dysfunction in Wistar rats: relevance to neuro-inflammation, neurotransmitters and Aβ

Kaur, Sunpreet / Raj, Khadga / Gupta, Y K / Singh, Shamsher

Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry

2021 Volume 26, Issue 4, Page(s) 495–510

Abstract: Alzheimer's disease (AD) is a multifactorial neurological disorder associated with neuropathological and neurobehavioral changes, like cognition and memory loss. Pathological hallmarks of AD comprise oxidative stress, formation of insoluble β-amyloid (Aβ) ...

Abstract	Alzheimer's disease (AD) is a multifactorial neurological disorder associated with neuropathological and neurobehavioral changes, like cognition and memory loss. Pathological hallmarks of AD comprise oxidative stress, formation of insoluble β-amyloid (Aβ) plaques, intracellular neurofibrillary tangles constituted by hyperphosphorylated tau protein (P-tau), neurotransmitters dysbalanced (DA, NE, 5-HT, GABA and Glutamate) and metal deposition. Chronic exposure to metals like aluminium and copper causes accumulation of Aβ plaques, promotes oxidative stress, neuro-inflammation, and degeneration of cholinergic neurons results in AD-like symptoms. In the present study, rats were administered with aluminium chloride (200 mg/kg p.o) and copper sulfate (0.5 mg/kg p.o) alone and in combination for 28 days. Allicin (10 and 20 mg/kg i.p) was administered from day 7 to day 28. Spatial and recognition memory impairment analysis was performed using Morris water maze, Probe trial, and Novel Object Recognition test. Animals were sacrificed on day 29, brain tissue was isolated, and its homogenate was used for biochemical (lipid peroxidation, nitrite, and glutathione), neuro-inflammatory (IL-1β, IL-6 and TNF- α), neurotransmitters (DA, NE, 5-HT, GABA and Glutamate), Aβ
MeSH term(s)	Aluminum Chloride/toxicity ; Amyloid beta-Peptides/genetics ; Amyloid beta-Peptides/metabolism ; Animals ; Cognitive Dysfunction/chemically induced ; Cognitive Dysfunction/drug therapy ; Copper Sulfate/toxicity ; Disulfides/chemistry ; Disulfides/pharmacology ; Glutathione ; Inflammation/drug therapy ; Learning/drug effects ; Lipid Peroxidation/drug effects ; Male ; Molecular Structure ; Neurotransmitter Agents/metabolism ; Nitrites ; Rats ; Rats, Wistar ; Sulfinic Acids/chemistry ; Sulfinic Acids/pharmacology
Chemical Substances	Amyloid beta-Peptides ; Disulfides ; Neurotransmitter Agents ; Nitrites ; Sulfinic Acids ; allicin (3C39BY17Y6) ; Aluminum Chloride (3CYT62D3GA) ; Glutathione (GAN16C9B8O) ; Copper Sulfate (LRX7AJ16DT)
Language	English
Publishing date	2021-05-22
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1464026-0
ISSN	1432-1327 ; 0949-8257
ISSN (online)	1432-1327
ISSN	0949-8257
DOI	10.1007/s00775-021-01866-8
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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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