Showing 15 results for Alzheimer
Gholamreza Chalabianloo, Mirtaghi Garooci Farshi, Ali Akbar Malekirad, Ali Hashemzadeh,
Volume 13, Issue 2 (6-2010)
Abstract
Background: Memory is one of the main functions that is impaired by neurological disorders. Noticing the susceptibility of memory to emotions, the effect of emotional states on memory in patients with alzheimer, brain tumor, and normal individuals was investigated in this study. Materials and Methods: Through Causal-Comparative study, 26 patients with alzheimer, 38 patients with brain tumor, and 30 normal individuals were selected and tested by a memory-related computerized task on explicit recall memory and implicit memory. Results: Patients with alzheimer showed a poor performance in memory tasks. They recognized more sad and threatening words in their explicit memory. Overall, patients with alzheimer and tumor in comparison with normal individuals indicated poorer explicit/implicit memory functions, respectively. Conclusion: Cognitive processes of patients with alzheimer are influenced when they encounter simple emotional stimulus.
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.
Ali Yaghoubi, Marziyeh Saghebjoo, Zia Fallah Mohammadi, Mehdi Hedayati, Akbar Hajizadeh Moghaddam,
Volume 18, Issue 11 (2-2016)
Abstract
Background: The Amyloid beta (Aβ) level increases in the brain of patients with Alzheimer's disease. The present study aimed to investigate the effects of eight weeks continuous training with low and high intensities on Aβ1-42 levels in hippocampus of Alzheimer model rats.
Materials and Methods: Fifty male Wistar rats (12 weeks old and mean weight 219.82±13.10 g) were divided into five groups including: healthy control, Alzheimer’s control, Alzheimer's low-intensity training, Alzheimer's high-intensity training and sham. To induce Alzheimer's disease, homocysteine is infused into the rats cerebroventricular (dose of 0.6M). Low intensity groups trained with 20m/min (50-55% VO2max) and high-intensity groups trained with 27m/min (75-80% VO2max), 60min/day, and five days per week on the treadmill. For data analysis, one-way ANOVA and post hoc Tukey test were performed (p<0.05).
Results: The Aβ1-42 levels in hippocampus of Alzheimer's control group was significantly higher than healthy control group (p=0.001) and in training groups with both low and high intensity was significantly lower than Alzheimer's control group (p=0.02). But no significant differences were found between two intensity (p=0.99).
Conclusion: It seems that continuous exercise training, through reducing the level of Aβ1-42 in hippocampus, can be useful for Alzheimer’s disease model rats and continuous training can be studied as a complementary therapy in Alzheimer's disease.
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.
Atabak Shahed, Ali Asghar Ravasi, Sirous Choubineh, Davar Khodadadi,
Volume 20, Issue 11 (2-2018)
Abstract
Abstract
Background: The aim of this study was to investigate the effect of four weeks exercise prior preparation before Alzheimer's induction on the levels of nerve growth factor and beta amyloid in the hippocampus of Wistar male rats
Materials and Methods: 84 male Wistar rats (8 weeks old) with a weighing average of 20 ± 195 grams from Pasteur Institute of Iran were prepared, and rats were randomly divided to two exercise (4 weeks aerobic training on a treadmill with a gradient of 0 degrees, 5 days a week for 4 weeks) and rest groups. Then, the rats of each group were randomly assigned to 3 sub groups of 14 numbers, injection Aβ1-42, control, and non-injected. 48 hours after the last exercise session, injections into the hippocampus amyloid beta or Dimethyl sulfoxide were performed. Seven days after surgery, the rats of each group were randomly sacrificed or subjected to behavioral testing. To determine the levels of of nerve growth factor and beta amyloid Sampling was performed from the hippocampus and plasma of animals, a Morris water maze test was used for spatial memory test. Kolmogorov-Smirnov test (KS) and analysis of variance were used to analyze the data.
Results: The results of one-way analysis of variance showed that there was a significant difference between the levels of amylohyd of hippocampus and NGF in different groups. Also, the results of the probe test for spatial memory showed that the time spent on the target circle in the Aβ1-42 injection group was significantly lower than the other groups (p≤ 0.01). Also, the exercise and exercise + sham groups had a significantly better performance than control group.
Conclusion: It seems that performing physical activity before induction of Alzheimer's in rats is a kind of countermeasures and preeclampsia with physiological disorders and progression of the disease.
Farhad Azimi, Marefat Siahkouhian, Farnaz Seifi-Skishahr, Roghayeh Afroundeh,
Volume 20, Issue 12 (3-2018)
Abstract
Abstract
Background: H2S plays a key role in the pathogenesis of the Alzheimer’s disease. The aim of the present study was to investigate the effects of 4 weeks of the special aerobic training after induction of Alzheimer’s disease by Aβ1-42 injection on CBS and SAM levels in hippocampus of Wistar male rats.
Materials and Methods: Twenty male Wistar rats (8 weeks old and weight 195 ± 20 g) were divided into four groups including: healthy control, Alzheimer’s control, Alzheimer’s + training and sham. To induce Alzheimer’s disease, Aβ1-42 was infused into the hippocampus of rats. Training group trained for 4-week. For data analysis, one-way ANOVA was used and Eta and Omega squared tests were used to determine the effect size (p<0.05).
Results: Findings revealed that 4 weeks of special aerobic training increased significantly the CBS and SAM levels in hippocampus of Alzheimer’s rats compared to the control Alzheimer’s rats ( ES=53; p= 0.007, ES= 92.22; p= 0.001). Also, we showed 4 weeks of special aerobic training increased CBS level in hippocampus of Alzheimer’s rats compared to the healthy cotrol group (ES= 44.07;
p= 0.014).
Conclusion: It seems that the special aerobic training can be used as a useful non-pharmacologically effective therapeutic treatment for Alzheimer's patients through positive regulation of hydrogen sulfide via CBS and SAM enzymes.
Azadeh Agahi, Gholamali Hamidi, Mahmoud Salami, Azam Alinaghipour, Reza Daneshvar Kakhaki, Masoud Soheili,
Volume 20, Issue 12 (3-2018)
Abstract
Abstract
Background: Alzheimer’s disease (AD) is a most common neurodegenerative disorder. The aim of this study was to investigate the effect of probiotic on cognitive function in patients with Alzheimer disease.
Materials and Methods: This clinical trial was conducted among 48 AD patients. The patients were randomly divided into two groups (n=23 in control group and n=25 in probiotic group) treating with capsules 500mg containing maltodextrine (control group) and probiotic supplementation (probiotic group) for 12 weeks. Mini-mental state examination (MMSE) and TYM test score was recorded in all subjects before and after treatment.
Results: After 12 weeks intervention, compared with the control group, the probiotic treated, patients with mild degree of Alzheimer disease showed an improvement in the MMSE, TYM score
(p < 0.0001).
Conclusion: Our current study demonstrated that probiotic consumption for 12 weeks positively affects cognitive function in mild degree of 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.
Samira Asgharzade, Mana Shojapour,
Volume 26, Issue 4 (11-2023)
Abstract
Background and Aim: Alzheimer's Disease (AD) is a progressive neurodegenerative disease characterized by loss of memory and multiple cognitive impairments.
Materials and Methods: In this study, key terms were searched in reputable Persian and English databases including DOAJ, PubMed, Google Scholar, LISTA (EBSCO), Embase, and Web of Science. Articles focusing on the molecular basis and pathogenesis of the disease, as well as biomarkers for Alzheimer's diagnosis, were reviewed. In this article, we have attempted a comprehensive review not only of the molecular basis of Alzheimer's disease from a molecular medical perspective but also to address numerous molecular diagnostic methods and biomarkers at both clinical and research levels in this disease.
Ethical Considerations: All Ethical principles in writing this article have principles been observed according to the instructions of National Ethics Committee and the COPE regulations
Findings: The results of this review study indicate that the major factors involved in the pathogenesis of Alzheimer's include beta-amyloid peptides, hyperphosphorylation of tau protein, and activation of inflammatory and oxidative stress pathways. Subsequently, this leads to synaptic loss, mitochondrial dysfunction, and proliferation of activated astrocytes and microglia, which are clinically manifested as memory loss in patients."
Conclusion: Although no precise diagnostic method exists for AD, current clinical recommendations for AD diagnosis include assessing tau protein and beta-amyloid (Aβ) peptides in cerebrospinal fluid, magnetic resonance imaging (MRI) for brain volume, and positron emission tomography (PET) scanning for Aβ plaques and/or glucose metabolism in the brain.
Mehdi Hajivand, Mohammad Fathi, Zinab Gorgin, Dr Raziyeh Rezaei,
Volume 26, Issue 6 (2-2024)
Abstract
Backgrand: Inflammation can cause damage to the central nervous system, leading to neuropathological diseases such as stroke, pain, schizophrenia, and Alzheimers. AIM2 is a member of the PYHIN hematopoietic nuclear protein family that binds to cytosolic DNA and activates caspase-1, one of the inflammatory-mediated caspases that activates pro-inflammatory cytokines. The aim of this research is to investigate the effect of a swimming training course on the expression of caspase-1 and AIM2 proteins in the hippocampus of male Wistar rats.
Method: The statistical population of this study included 16 male Wistar rats (6 weeks) divided into two groups: a group without training and an endurance training group. Eight rats were placed in each group. The group without training did not engage in any sports activities, while the training group participated in a swimming training session. After a 4-day familiarization period, the rats swam for 30 minutes from the fifth day. Independent T-test was used to evaluate the interventions, and all statistical calculations were done using SPSS statistical software.
Results: The results of this research showed that exercise caused a significant decrease in the level of caspase-1 and AIM2 proteins in the hippocampus of male Wistar rats.
Discussion: Overall, this study suggests that endurance swimming training can effectively reduce caspase-1 and AIM2 proteins. Therefore, it is possible that exercise, by reducing inflammatory factors, can be a potential treatment for diseases caused by inflammation, such as sclerosis, diabetes, cancer, and Alzheimers.
Maryam Keshvari, Ali Heidarianpour, Farzaneh Chehelcheraghi,
Volume 27, Issue 5 (12-2024)
Abstract
Introduction: The thickness of the molecular and pyramidal layers in the hippocampus represents a pivotal aspect of Alzheimer's research. This study was conducted to investigate the effect of swimming endurance, resistance, and combined exercises on the molecular and pyramidal layers of the hippocampus tissue thickness of Alzheimer's rats.
Methods: In this experimental study, 40 large white Wistar laboratory rats (6 weeks old; Weight 180-200 g) were randomly and equally divided into five groups: healthy control, Alzheimer's control, endurance, resistance, and combined. Alzheimer's disease was induced by intraperitoneal injection of trimethyltin chloride (8 mg/kg). Two weeks after the injection and confirmation of Alzheimer's induction, the training protocols of endurance (5-sessions/week, the first to the fourth week incrementally from 5-15-min to 45-min of swimming, the fifth to the twelfth week 60-min of swimming), resistance (5-sessions/week, The first week of familiarization with the exercise, week 2; 30%, week3-5; 70-90%, week6-8; 100-110%, week9-10; 120-130%, and week11-12; 140-150% of body weight), combined (2 resistance sessions/week and three endurance sessions/week) was performed for 12 weeks. Forty-eight hours post-intervention, animals were dissected, and hippocampus tissue was harvested. Finally, the data were analyzed at the significance level of P < 0.05.
Results: The thickness of the molecular and pyramidal layers of the hippocampal tissue of Alzheimer's animals decreased compared to healthy animals, and all three endurance, resistance, and combined exercise protocols increased layers (P < 0.001). However, the increase in the molecular and pyramidal layers thickness of the hippocampal tissue of combined group rats compared to the endurance and resistance group had a greater increase (P < 0.01).
Conclusions: These findings highlight the changes in the thickness of the hippocampal tissue layers concerning Alzheimer's pathology and the effect of combined exercises on this parameter. While exercise may have positively affected hippocampal volume and synaptic plasticity, more research is needed to fully understand the impact of exercise on hippocampal layer thickness in Alzheimer's.
