Impaired memory and evidence of histopathology in CA1 pyramidal neurons through injection of Aβ1-42 peptides into the frontal cortices of rat

Introduction: Alzheimer's disease (AD) is one of the most common neurodegenerative disorders, which has much benefited from animal models to find the basics of its pathophysiology. In our previous work (Haghani, Shabani, Javan, Motamedi, & Janahmadi, 2012), a non-transgenic rat model of AD was used in electrophysiological studies. However, we did not investigate the histological aspects in the mentioned study. Methods: An AD model was developed through bilateral injection of amyloid-β peptides (Aβ) into the frontal cortices. Behavioral and histological methods were used to assess alterations in the memory and (ultra)structures. Furthermore, melatonin has been administered to assess its efficacy on this AD model. Results: Passive avoidance showed a progressive decline in the memory following Aβ injection. Furthermore, Nissl staining showed that Aβ neurotoxicity caused shrinkage of the CA1 pyramidal neurons. Neurodegeneration was clearly evident from Fluoro-jade labeled neurons in Aβ treated rats. Moreover, higher NF-κB immunoreactive CA1 pyramidal neurons were remarkably observed in Aβ treated rats. Ultrastructural analysis using electron microscopy also showed the evidence of subcellular abnormalities. Melatonin treatment in this model of AD prevented Aβ- induced increased NF-κB from immunoreaction and neurodegeneration. Discussion: This study suggests that injection of Aβ into the frontal cortices results in the memory decline and histochemical disturbances in CA1 pyramidal neurons. Furthermore, melatonin can prevent several histological changes induced by Aβ

A Review on Brain Evolution and Development

Development of human brain is the essential process in the prenatal period of human growth. The total surface of human brain area is 1820 cm2, and the average cortical thickness is 2.7 mm. We reviewed and referred to several articles in this field. Comparative studies of the primate's brain show that there are general architectural basis governing the brain growth and evolutionary development. In this study, it is discussed about the human brain development with highlighting on the main mechanisms in the embryonic stage and early postnatal life as well as the general architectural values in brain evolution from primates to now. It is suggested that neurodevelopment involves some genetic bases in the neural stem cells proliferation, cortical neurons migration, cerebral cortex folding, synaptogenesis, gliogenesis, and myelination of neural fibers

Neuroprotective Effects of Carnosic Acid in an Experimental Model of Alzheimer’s Disease in Rats

Objective: Alzheimer’s disease is the most common type of neurodegenerative disorder.It has been suggested that oxidative stress can be one of the pathological mechanisms ofthis disease. Carnosic acid (CA) is an effective antioxidant substance and recent studieshave shown that its electrophilic compounds play a role in reversing oxidative stress. Thuswe tried to find out whether CA administration protects hippocampal neurons, preventingneurodegeneration in rats.Materials and Methods: Animals were divided into four groups: Sham-operated (sham),CA-pretreated sham-operated (sham+CA), untreated lesion (lesion) and CA-pretreatedlesion (lesion+CA). Animals in all groups received vehicle or vehicle plus CA (CA: 10mg/kg) intra-peritoneally one hour before surgery, again the same solution injected 3-4hours after surgery (CA: 3 mg/kg) and repeated each afternoon for 12 days. A lesionwas made by bilateral intra-hippocampal injection of 4 μl of beta amyloid protein (1.5nmol/μl) or vehicle in each side. 14 days after surgery, the brains were extracted forhistochemical studies. Data was expressed as mean ± SEM and analyzed using SPSSstatistical software.Results: Results showed that pretreatment with carnosic acid can reduce cellular deathin the cornu ammonis 1 (CA1) region of the hippocampus in the lesion+CA group, as comparedwith the lesion group.Conclusion: Carnosic acid may be useful in protecting against beta amyloid-induced neurodegenerationin the hippocampus

Neuroprotective Effects of Trolox, Human Chorionic Gonadotropin, and Carnosic Acid on Hippocampal Neurodegeneration After Ischemiareperfusion Injury

INTRODUCTION: One of the serious complications of stroke is memory impairment, which is considered as one of the complications of reperfusion of tissue. The present study was designed to compare the effect of administration of Trolox, carnosic acid and Human Chorionic Gonadotropin (HCG) immediately after reperfusion of the stroke tissue on the memory and hippocampal histology. METHOD: Ischemia-Reperfusion Model (IRI) was created by bilateral occlusion of the common carotid artery for 15 minutes and the first dose was administered immediately after reperfusion. 10 days after ischemia, passive avoidance memory test and apoptotic protein levels were evaluated. RESULTS: Cerebral Ischemia perfusion reduced the time of latency in entering the dark box in the ischemic group. Administration of Trolox and HCG increased this latency time, while treatment with carnosic acid had no effect. Also, IRI significantly reduced the number of healthy cells in the hippocampus. Administration of Trolox, carnosic acid and HCG increased the number of healthy cells and decreased the expression of Caspase-3 and Bax, but significantly increased the expression of Bcl-2 compared to the ischemic group. CONCLUSION: Findings indicate the beneficial effects of HCG and Trolox on the improvement of memory and the number of healthy cells in the hippocampal region. It is worth noting that the amount of apoptosis in the hippocampus was significantly reduced by Trolox, HCG and Carnosic aci

Neuroprotective Effects of Trolox, Human Chorionic Gonadotropin, and Carnosic Acid on Hippocampal Neurodegeneration After Ischemia-reperfusion Injury.

INTRODUCTION: One of the serious complications of stroke is memory impairment, which is considered as one of the complications of reperfusion of tissue. The present study was designed to compare the effect of administration of Trolox, carnosic acid and Human Chorionic Gonadotropin (HCG) immediately after reperfusion of the stroke tissue on the memory and hippocampal histology. METHOD: Ischemia reperfusion model (IRI) was created by bilateral occlusion of the common carotid artery for 15 minutes and the first dose was administered immediately after reperfusion. 10 days after ischemia, passive avoidance memory test and apoptotic protein levels were evaluated. RESULTS: Cerebral Ischemia perfusion reduced the time of latency in entering the dark box in the ischemic group. Administration of Trolox and HCG increased this latency time, while treatment with carnosic acid had no effect. Also, IRI significantly reduced the number of healthy cells in the hippocampus. Administration of Trolox, carnosic acid and HCG increased the number of healthy cells and decreased the expression of Caspase-3 and Bax, but significantly increased expression of Bcl-2 compared to the ischemic group. CONCLUSION: Findings indicate the beneficial effects of HCG and Trolox on the improvement of memory and the number of healthy cells in the hippocampal region. It is worth noting that the amount of apoptosis in the hippocampus was significantly reduced by Trolox, HCG and Carnosic acid