Naringenin improves learning and memory in an Alzheimer's disease rat model: Insights into the underlying mechanisms

Background: Alzheimer’s Disease (AD) is a chronic neurodegenerative disease characterized by abnormal protein accumulation, synaptic dysfunction, and cognitive impairment. Peroxisome Proliferator-Activated Receptor-γ (PPARγ) play a crucial role in regulating insulin sensitivity and may serve as potential therapeutic targets for AD. Pioglitazone (PIOG), as a PPARγ agonist, reduces β-amyloid and tau proteins, and inhibits neuroinflammation. Objective: This study aims to evaluate the effects of PIOG chronic administration on learning and memory in rat model of Streptozotocin (STZ)-induced AD Methods: Forty-two male Wistar rats were divided into two groups: A. Normal rats divided into three subgroups of Control, Dimethyl Sulfoxide (DMSO), and PIOG; and B. AD rats divided into four subgroups of Vehicle, STZ, STZ+DMSO and STZ+PIOG. The last two AD subgroups received 0.2 mL DMSO and PIOG (10 mg/kg per day) for 21 days. For induction of AD, STZ (3 mg/kg, 10 μl per injection site) were administered into lateral ventricles. All rates were trained under the Morris water maze task. Findings: PIOG impaired the spatial learning and memory in normal rats. Intracerebroventricular injection of STZ significantly increased escape latency and swimming time to find the hidden platform compared to the control group (P<0.05). The amnesic effect of STZ was prevented by PIOG administration such that the escape latency and swimming time to find the hidden platform in the STZ+PIOG group were significantly lower than in the STZ+DMSO group (P<0.05). Conversely, the percentage of time spent and distance swimming in the target quadrant in the probe test in the STZ+ PIOG group rats were significantly higher than those in the STZ + DMSO group. Conclusion: PIOG administration impaired spatial learning and memory in normal rats, but improved learning and memory in rats with STZ-induced AD. It can be useful for treatment of cognitive impairment in AD patients.

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Subtle learning and memory impairment in an idiopathic rat model of Alzheimer's disease utilizing cholinergic depletions and β-amyloid

Brain Research ◽

10.1016/j.brainres.2016.05.033 ◽

2016 ◽

Vol 1646 ◽

pp. 12-24 ◽

Cited By ~ 9

Author(s):

S.H. Deibel ◽

N. Weishaupt ◽

A.M. Regis ◽

N.S. Hong ◽

R.J. Keeley ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Learning And Memory ◽

Rat Model ◽

Memory Impairment ◽

Model Of Alzheimer’S Disease ◽

Β Amyloid

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The Effect of Cannabidiol Coated by Nano-Chitosan on Learning and Memory, Hippocampal CB1 and CB2 Levels, and Amyloid Plaques in an Alzheimer’s Disease Rat Model

Neuropsychobiology ◽

10.1159/000519534 ◽

2021 ◽

pp. 1-13

Author(s):

Mohammadali Amini ◽

Zohreh Abdolmaleki

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Protein Expression ◽

Learning And Memory ◽

Rat Model ◽

Cannabinoid Receptor ◽

Amyloid Plaques ◽

Receptor Type ◽

Cannabinoid Receptor Type 1

Introduction: Using nanoparticle (NP) drugs can have better effects on the target tissue in various diseases. Alzheimer’s disease (AD) is one of the degenerative neurological diseases that due to its high prevalence, requires the use of more appropriate treatments. Therefore, the aim of this study was consideration of the effect of cannabidiol (CBD) coated by nano-chitosan on learning and memory, hippocampal cannabinoid receptor type 1 (CB1) and cannabinoid receptor type 1 (CB2) levels, and amyloid plaques in an AD rat model. Material and Methods: Thirty-five male Wistar rats were randomly divided into 5 groups (n = 7 in each): control, Alzheimer’s disease model that received the beta-amyloid (Aβ) peptide (Alz), Alz + nano-chitosan (NP) Alz + CBD, and Alz + NP + CBD. Alz was induced by injection of the Aβ1-42 peptide into the hippocampal area cornu ammonis1. After confirmation of Alz, 1 μL of CBD and NP + CBD were administered by oral gavage daily in rats for 1 month. The Morris water maze (MWM) test was used to assess learning and memory of animals. Cresyl violet staining was used for consideration of dead cells. Gene and protein expression of CB1 and CB2 was performed by real-time PCR and immunohistochemistry methods. Results: Induction of Alz significantly increased Aβ plaques and dead cells compared to the control group (p < 0.001). Results of MWM in the day test show that Alz + NP + CBD significantly decrease escape latency (p < 0.01), travelled distance (p < 0.001), and significantly increased spending time (p < 0.001) compared to the Alz group. Protein expression of CB1 and CB2 significantly increased in Alz + CBD and Alz + NP + CBD compared to the Alz group (p < 0.05). Conclusion: It seems that CBD coated by nano-chitosan has good potential for reducing Aβ plaques, increasing brain CB1 and levels CB2, and improving learning and memory in Alz rats.

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Riluzole ameliorates learning and memory deficits in Aβ25-35-induced rat model of Alzheimer’s disease and is independent of cholinoceptor activation

Biomedicine & Pharmacotherapy ◽

10.1016/j.biopha.2016.12.067 ◽

2017 ◽

Vol 87 ◽

pp. 135-144 ◽

Cited By ~ 22

Author(s):

Zahra Mokhtari ◽

Tourandokht Baluchnejadmojarad ◽

Farnaz Nikbakht ◽

Monireh Mansouri ◽

Mehrdad Roghani

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Learning And Memory ◽

Rat Model ◽

Memory Deficits ◽

Model Of Alzheimer’S Disease ◽

Learning And Memory Deficits

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Icariin Attenuates Synaptic and Cognitive Deficits in an Aβ1–42-Induced Rat Model of Alzheimer’s Disease

BioMed Research International ◽

10.1155/2017/7464872 ◽

2017 ◽

Vol 2017 ◽

pp. 1-12 ◽

Cited By ~ 22

Author(s):

Chenxia Sheng ◽

Panpan Xu ◽

Kexin Zhou ◽

Dan Deng ◽

Chunhu Zhang ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Synaptic Plasticity ◽

Learning And Memory ◽

Rat Model ◽

Intragastric Administration ◽

Neuroprotective Effects ◽

Treatment And Prevention ◽

Model Of Alzheimer’S Disease ◽

Epimedium Sagittatum

Icariin (ICA), a prenylated flavanol glycoside present in abundant quantities in Epimedium sagittatum, has shown promise in the treatment and prevention of Alzheimer’s disease. Damage to synaptic plasticity induced by amyloid-beta-mediated neurotoxicity is considered a main pathological mechanism driving the learning and memory deficits present in patients with Alzheimer’s disease. This study investigated the neuroprotective effects of icariin in an Aβ1–42-induced rat model of Alzheimer’s disease. Our results showed that Aβ1–42 injection induced loss of learning and memory behaviour in the Morris water maze, which could be reversed with intragastric administration of ICA. Furthermore, ICA reversed decreases in PSD-95, BDNF, pTrkB, pAkt, and pCREB expressions and prevented deterioration of synaptic interface structure. These findings indicate that ICA may improve synaptic plasticity through the BDNF/TrkB/Akt pathway and provide further evidence for its clinical application to improve learning and memory in patients with Alzheimer’s disease.

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