Showing 7 results for Alzheimer’s Disease
Nasser Parsa,
Volume 14, Issue 2 (5-2011)
Abstract
Alzheimer’s disease is one of the most common causes of loss of mental function broadly known as “Dementia”. Alzheimer’s disease affects approximately 2% (6.5 Million) of people in the developed countries and responsible for over 100,000 death per year in USA Alzheimer’s disease usually occurs between sixth to ninth decade and its progressive deterioration comprised of gradual destruction of memory, judgment, language, reasons in addition to behavioral alterations. Microscopic biopsy shows cortical atrophy along with ventricular enlargement of the brain. These clinical manifestations reflect the neurotic degeneration in cerebral cortex, especially, the temporo-parietal cortex and the hippocampus. Pathological abnormalities of Alzheimer’s disease include brain deposition of two fibrillary proteins. These two are known as Beta-amyloid proteins containing Apolipoprotein E and Tau proteins. Alzheimer’s disease affects primarily cholinergic neurons, therefore, treatment is followed by specific drugs that inhibit the degradation of acetylcholine within synapses. Current medications only treat the cognitive symptoms but not the underlying disorder. Several lines of ongoing research are showing promising scientific results. These include, uncovering the biological markers for early detection and developing new effective drugs. Also, new approaches have been employed to block the molecular processes that lead to this disease. Moreover, many clinicians are exploring alternative pathways for Alzheimer’s disease treatment, such as good diet along with mental and physical exercise as preventive methods.
Mohsen Soosanabadi Farahani, Kourosh Kamali, Masoud Karimlou, Mehdi Banan, Hamid Reza Khorram Khorshid,
Volume 16, Issue 6 (9-2013)
Abstract
Background: There is abundant evidence indicating that inflammatory mechanisms within the central nervous system contribute to cognitive impairment via cytokine-mediated interactions between neurons and glial cells. BAT1, a member of the DEAD-box family of RNA helicases, appears to regulate the production of inflammatory cytokines associated with AD pathology. In the current study BAT1 -22 promoter polymorphism was analyzed in AD and control subjects.
Materials and Methods: In this case-control study, genomic DNA from peripheral blood samples of 153 Alzheimer’s patients and 153 healthy controls was extracted using salting-out method. DNA analysis was performed by PCR-RFLP method and p<0.05 was considered statistically significant.
Results: After genotyping and statistical analysis the results failed to show any association between BAT1 -22 promoter polymorphism and sporadic Alzheimer’s disease.
Conclusion: BAT1 -22 is not associated with Alzheimer’s disease in Iranian population and so has no effect on predisposition to sporadic Alzheimer’s disease.
Tayyebeh Khoshbakht, Mohsen Soosanabadi, Masoud Karimlou, Maryem Neishaboury, Hamid Reza Khorram Khorshid,
Volume 17, Issue 7 (10-2014)
Abstract
Background: Interleukin-16 (IL16) is an important regulator of T cell activation and was reported to act as achemo-attractant agent. There are evidences that IL16 can control the neuroinflammatory processes in Alzheimer’s disease (AD). This study was performed to show whether the IL-16 genepolymorphism, rs11556218 is associated with the risk of sporadic AD in Iranian population.
Materials and Methods: Totally, 148 AD patients and 137non-dementia controls were recruited in this case-control study. Genotyping of rs11556218 T/Gpolymorphism was performed by PCR-RFLP method using the NdeI restriction enzyme.
Results: Statistical analysis of rs11556218 genotypes showed a protective effect against AD in the heterozygote genotype (p=0.001, OR=0.16(0.1-0.28)). Frequency of rs11556218 allele T was higher in patients than controls (p=0.001, OR=0.32(0.21-0.49)).
Conclusion: Our results indicate thatrs11556218 polymorphism has a protective role in the development of sporadic AD in Iranian population.
Seyed Mahmoud Tabatabaei, Gholamreza Chalabianloo, Neda Seyedi,
Volume 20, Issue 10 (1-2018)
Abstract
Abstract
Background: The activation of inflammatory cascades reactions has been consistently demonstrated in the pathophysiology of Alzheimer’s disease (AD). Among several neuroinflammatory mechanisms, the tumor necrosis factor (TNF) signaling system has a central role in this process. The abnormal production of inflammatory factors may accompany the progression from mild cognitive impairment (MCI) to dementia. We aimed to examine serum levels of soluble TNF receptor (sTNFR1) in patients with MCI and AD as compared to cognitively unimpaired elderly subjects. We further aimed to investigate whether abnormal levels of these cytokines predict the progression from MCI to AD upon follow up.
Materials and Methods: We utilized cross-sectional determination of serum levels of sTNFR1 (ELISA method) in a test group comprising 150 older adults (30 AD, 60 MCI, and 60 healthy controls), and longitudinal reassessment of clinical status after12 months.
Results: At baseline, there were statistically significant differences in serum sTNFR1 between patients with MCI and AD and controls (p< 0.05). Also, patients with MCI who had more disorder in diagnostic functions and progressed to AD after one year, had significantly higher serum sTNFR1 levels as opposed to patients who retained the diagnosis of MCI upon follow up (p=0.03).
Conclusion: The results showed that abnormal activation of TNF signaling system, represented by increased expression of sTNFR1, is associated with a higher risk of progression from MCI to AD.
Nastaran Zamani, Ahmad Ali Moazedi,
Volume 22, Issue 6 (1-2020)
Abstract
Background and Aim: Alzheimer’s disease is the most common causes of dementia among the elderly people. The aim of this study was to evaluate the synergistic effects of memantine and vitamin D on spatial learning and memory impairment in adult male rat model of Alzheimer's disease.
Methods & Materials: In this experimental study, male Wistar rats were randomly divided into nine groups (n=7): 1= Control, 2= NBM lesion (received bilateral electric lesion of NBM), 3= Sham (the electrode was entered into the NBM with no electric lesion), 4= NBM lesion+ Vehicle Memantine (received saline), 5= NBM lesion+ Vehicle Vitamin D (received saline), 6= NBM lesion+ Vehicle Memantine+ Vehicle Vitamin D (received saline plus sesame oil), 7= NBM lesion+ Vitamin D; 8= NBM lesion+Memantine, and 9= NBM lesion+Vitamin D+Memantine. After one week, the rats were trained to perform the Y-maze task for five days. Twenty five days after training, a retention test was performed to evaluate their long-term memory.
Ethical Considerations: This study with research ethics code of “EE/ 97, 24, 3061243/scu.ac.ir” was approved by the Research Ethics Committee of Shahid Chamran University of Ahvaz In Iran.
Results: Bilateral NBM lesion reduced spatial learning in comparison with control and sham groups. No effect on spatial learning was observed in NBM lesion+ Vehicle Memantine and NBM lesion+ Vehicle Vitamin D groups compared to the NBM lesion group. Spatial learning and memory in NBM lesion +Vitamin D+Memantine group (P<0.001) was significantly improved compared to NBM lesion+Vitamin D (P<0.01) and NBM lesion+Memantine (P<0.05) groups. Moreover, no significant difference was observed between the results in the 5th day of training and the memory retention at the 30th day.
Conclusion: Co-administration of memantine and vitamin D is more effective than memantine or vitamin D alone in spatial learning and memory improvement in rat model of Alzheimer's disease.
Zakiyeh Gharib, Naser Sanchooli, Nima Sanadgol,
Volume 23, Issue 2 (5-2020)
Abstract
Background and Aim: This study aimed to investigate the association between Endoplasmic Reticulum autophagy (ER-phagy) and Alzheimer’s Disease (AD) by analyzing the expression patterns of related genes in animal models.
Methods & Materials: Microarray data of AD patients’ brain tissues were extracted from the Gene Expression Omnibus (GEO) database. These data were first analyzed in GEO2R online tool. Then, the expression of ER-phagy related genes were isolated and the protein interaction networks were plotted by STRING database for the genes with increased expression. Finally, the relationship between the genes that had significant increased expression were designed, and the expression of new identified genes in each study was examined.
Ethical Considerations: All ethical principles were considered in this article.
Results: Genes involved in ER-phagy showed a sporadic expression in different AD models. An increase in the expression of ER-phagy regulatory 1 (FAM134B) gene was observed in studies with the mutation in both Microtubule-associated Protein Tau (MAPT) and Amyloid Precursor Protein (APP) genes. Increase in the expression of NPC intracellular cholesterol transporter 1 (NPC1) gene was observed in two studies that had mutations in APP, Presenilin 1 (PSEN1) and MAPT genes. Moreover, SEC62 homolog and Cell Cycle Progression 1 (CCPG1) genes both showed decreased expression in one study. Finally, the expression of Reticulon 3 (RTN3) was not significant in any of the studies.
Conclusion: The genes involved in ER-phagy have a sporadic expression in AD models, where only two genes FAM134B and NPC1 are involved in AD. The FAM134B gene seems to interact with the Wnk1 gene, which plays a role in cell survival and proliferation, in the hippocampus and forebrain. It also interacts with the Map1lc3b gene, which has a role in phagosome deletion and protein ubiquitination, in the forebrain. It also interacts with the Map1lc3b gene, which has a role in phagosome deletion and protein ubiquitination, in the forebrain. NPC1 had interaction with the Abcg1 gene, which activates lipid homeostasis, in the subventricular zone.
Fatemeh Heidari Soureshjani, Majid Kheirollahi, Parichehreh Yaghmaei, Fattah Sotoodehnejadnematalahi,
Volume 23, Issue 4 (9-2020)
Abstract
Background and Aim: Alzheimer's Disease (AD) is a neurodegenerative brain disease that gradually destroys memory and cognitive skills. The disease is caused by the formation of beta-amyloid plaques, oxidative stress, dysfunctions in the cholinergic system, neuronal killing inflammation, and ultimately brain atrophy. Donepezil and hyoscyamoside have inhibitory effects on these pathogens; therefore, their impact on the learning process of Alzheimer’s rats in the Morris Water Maze was investigated.
Methods & Materials: In the present experimental study, 60 male rats of Wistar breed with approximately 7 weeks age within the control group (rats that received normal water and food), the PBS group (underwent surgery), PBS group (received solvent Aβ), the first Alzheimer›s group (animals that received beta-amyloid by Alzheimer’s surgery, second Alzheimer’s group (after Alzheimer’s surgery, they received 1 cc of normal saline daily, and treatment groups that treated the rats with beta-amyloid after Alzheimer. In the hyoscyamoside group, they received 10 mg/kg daily of hyoscyamoside for 28 days. The donepezil group received it 4 mg/kg daily for 28 days by gavage. The Morris Water Maze test was used to evaluate learning and memory. Data were analyzed by ANOVA statistical analysis and Post Hoc test.
Ethical Considerations: The Ethics Committee in Biomedical Research, Islamic Azad University, Science and Research Branch approved the research (Code: IR.IAU.SRB.REC 1397.057)
Results: Beta-amyloid injection caused extensive damage to memory. The treatment groups with hyoscyamoside and donepezil spent less time and distance with a significant level (P<0.001) than the group of Alzheimer’s patients to find the hidden platform. In the reminder phase, where the previously hidden platform was located, they spent more time, with a significant level (P<0.001) in the local quarter.
Conclusion: Treatment of rats with hyoscyamoside and donepezil improved spatial memory in Alzheimer’s rats. They appear to play a significant role in the prevention and treatment of Alzheimer’s disease.
